Eating Disorders

Eating disorders are a group of psychiatric conditions characterized by persistent disturbances in eating behavior and related thoughts and emotions, including anorexia nervosa, bulimia nervosa, and binge eating disorder, that significantly impair physical health and psychosocial functioning.

Exam domain	One-glance essentials
Definition / diagnosis	Psychiatric disorders with disturbed eating or weight-control behaviour ^[1] Core syndromes include anorexia nervosa, bulimia nervosa and binge-eating disorder ^[1]
Epidemiology / risks	Female sex, adolescence, dieting and body-image pressure increase risk ^[1] Perfectionism, trauma and family/genetic vulnerability contribute ^[1]
Core mechanism	Restriction, bingeing and compensatory behaviour become self-reinforcing ^[1] Starvation alters cognition, endocrine axes and cardiovascular function ^[1]
Clinical picture	Weight loss, fear of weight gain, bingeing, vomiting or compulsive exercise ^[1] Bradycardia, amenorrhoea, dental erosion and parotid enlargement are clues ^[1]
Investigations	Assess BMI trajectory, vitals, ECG, glucose and electrolytes including phosphate ^[2] Screen suicide risk, purging, exercise and medical instability ^[2]
Management	Restore nutrition with psychological and dietetic treatment ^[3] Admit for severe instability; replace electrolytes and prevent refeeding syndrome ^[3]
Complications	Arrhythmia, osteoporosis, infertility and multiorgan effects ^[4] Suicide and refeeding syndrome are major causes of harm ^[4]
Prevention / follow-up	Promote early recognition and avoid weight-stigmatising care ^[3] Relapse planning and family-based support reduce chronicity ^[3]
Exam traps	*Normal BMI does not exclude a dangerous eating disorder* ^[2] Correct potassium urgently, but anticipate phosphate fall during refeeding ^[3]

References

^[1] Lecture slides: GC 167. I feel very nervous Anxiety disorders.pdf (general psychiatric context)

^[2] Senior notes: ryanho-psych.md (Sections 9.1, 9.1.1, 9.1.2 — Eating Disorders, Anorexia Nervosa diagnostic criteria, Bulimia Nervosa diagnostic criteria, investigation tables, risk assessment, and differential diagnosis)

^[3] Senior notes: ryanho-psych.md (Sections 9.1, 9.1.1, 9.1.2 — Eating Disorders: Approach to Management, Nutritional rehabilitation, Psychotherapy, Medications, Maudsley Family Therapy, CBT-E, MANTRA, Bulimia Nervosa management)

^[4] Senior notes: ryanho-psych.md (Sections 9.1, 9.1.1, 9.1.2 — Eating Disorders: Physical features of AN, Abnormalities on investigation, BMI risk stratification, Clinical features of BN, Course and prognosis, Mortality, Refeeding syndrome, Complications)

Eating disorders are a group of psychiatric conditions characterised by persistent disturbances in eating behaviour and related thoughts/emotions that significantly impair physical health and psychosocial functioning. They share a distinctive core psychopathology: over-evaluation of weight and shape, where patients judge their self-worth largely — or even exclusively — in terms of their body shape, weight, and their ability to control them ^[1]^[2].

Let's break the term down:

"Eating" = obviously about food intake
"Disorder" = a disruption of normal function

But the name undersells it. These are not simply "problems with food." They are severe neuropsychiatric illnesses with the highest mortality of any psychiatric disorder class (in the case of anorexia nervosa), driven by complex gene-environment interactions, neurobiological dysfunction, and powerful cognitive distortions ^[2].

Core Psychopathology — The Unifying Feature

All eating disorders share an over-evaluation of weight and shape: patients define their self-worth almost entirely by their ability to control weight, shape, and eating. This is the engine that drives restrictive eating, binge eating, and compensatory behaviours. If you understand this one concept, the rest of the clinical picture falls into place logically.

Key principle: Individuals often migrate between diagnostic categories (AN → BN → OSFED and back). This suggests they share a common underlying pathophysiology, and the boundaries between them are largely arbitrary — think of them as a spectrum rather than discrete boxes ^[2].

2. Epidemiology

Incidence: 4–5 per 100,000 population per year ^[2]
Prevalence: ~250 per 100,000 in females vs ~22 per 100,000 in males; approximately 0.5–1% of females aged 13–35 years ^[2]
Hong Kong data: Disordered eating (subthreshold) is present in 3.9% of males and 6.5% of females aged 10–21 years — this is a significant reservoir of at-risk individuals ^[2]
Sex ratio: F:M ≈ 10:1 — male AN is often underreported and stigmatised ^[2]
Age of onset: Usually within a few years of menarche; 40% onset between 15–19 years. AN is the 3rd most common chronic illness in teenage girls (after obesity and asthma) ^[2]
Culture-bound: Lower prevalence in non-industrialised countries and among African-Americans; higher in Western/Westernised societies ^[2]
Occupational risk: Prevalence of 4–6% among models and ballet dancers ^[2]
Comorbidities: Anxiety disorders, OCD, body dysmorphic disorder, depressive disorders (3/4 with lifetime history), PTSD, substance abuse disorders ^[2]
Mortality: Highest mortality of ALL psychiatric disorders
- Standardised Mortality Ratio (SMR): 23.14× ^[2]
- Average age at death: 34 years
- Major causes of death: suicide (32%), anorexia itself (19%), cancer (11%) ^[2]

Incidence: ~12 per 100,000 per year ^[2]
Prevalence: ~1,000 per 100,000 in females; 2–5% of females aged 13–35 years ^[2]
Sex ratio: F:M ≈ 10:1 ^[2]
Mean onset: ~18 years, with 30% having prior AN and one-third prior obesity ^[2]
Comorbidities: Depression (50%), anxiety disorders/OCD, substance abuse, impulsivity, borderline personality disorder ^[2]

Prevalence: ~2–3.5% lifetime; the most common eating disorder overall
Sex ratio: More equal than AN/BN — approximately F:M ≈ 3:2
Strong association with obesity: Found in 20–30% of patients seeking weight-loss treatment
Comorbidities: Mood disorders, anxiety disorders, metabolic syndrome

OSFED (previously "Eating Disorder Not Otherwise Specified" / EDNOS) accounts for the majority of eating disorder presentations — 50–70% ^[2]

Hong Kong Context

While classical AN with fat-phobia is the textbook presentation, studies from Hong Kong and other Asian populations have noted a subset of AN patients who lack fat-phobia ("non-fat-phobic AN") and instead attribute food restriction to epigastric bloating, loss of appetite, or other somatic complaints. This is important for clinical recognition in the local population.

3. Classification

The DSM-5 and ICD-11 both classify eating disorders, but the DSM-5 framework is the one most heavily examined ^[2]:

DSM-5 Feeding and Eating Disorders	ICD-10/11 Equivalents
Anorexia Nervosa	Anorexia Nervosa
Bulimia Nervosa	Bulimia Nervosa
Binge Eating Disorder	Binge Eating Disorder (ICD-11)
Avoidant/Restrictive Food Intake Disorder (ARFID)	Atypical Anorexia Nervosa
Other Specified Feeding or Eating Disorder (OSFED)	Atypical Bulimia Nervosa
Unspecified Feeding or Eating Disorder	Other eating disorders (e.g. pica)
Pica	Eating disorder, unspecified
Rumination Disorder	—

Restricting type: Weight loss accomplished primarily through dieting, fasting, and/or excessive exercise — no recurrent binge-eating or purging in the last 3 months
Binge-eating/Purging type: Recurrent episodes of binge eating or purging behaviour (self-induced vomiting, laxative/diuretic misuse) during the last 3 months

AN severity — based on BMI:

Severity	BMI (kg/m²)
Mild	≥ 17
Moderate	16–16.99
Severe	15–15.99
Extreme	< 15

BN severity — based on frequency of compensatory behaviours per week:

Severity	Compensatory behaviours/week
Mild	1–3
Moderate	4–7
Severe	8–13
Extreme	≥ 14

Important concept: AN and BN are not static diagnoses. There is considerable overlap and migration between categories — a patient may begin with AN restricting type, develop binge-eating, transition to BN, and later meet criteria for OSFED. The underlying over-evaluation of weight and shape is the constant thread ^[2].

4. Anatomy and Function: Key Neurobiological Systems

To understand eating disorders, you need to understand three interacting systems:

The hypothalamus is the master regulator of appetite, energy homeostasis, and reproductive function
In starvation (as in AN), the hypothalamus shuts down non-essential functions to conserve energy:
- ↓ GnRH pulsatility → ↓ LH/FSH → amenorrhoea (females) / loss of libido and impotence (males) ^[2]
- This is a functional, adaptive response to energy deficit — the body "decides" reproduction is not safe when starving
Why does amenorrhoea occur early? Because GnRH pulsatility is exquisitely sensitive to energy balance — even modest caloric deficit can suppress it. This is why amenorrhoea can occur before dramatic weight loss is evident ^[2]

Starvation → chronic physiological stress → ↑ CRH → ↑ cortisol
Patients with AN have elevated cortisol and dexamethasone non-suppression (pseudo-Cushing's) ^[2]
Hypercortisolaemia contributes to osteoporosis, immunosuppression, and mood disturbance

Serotonin (5-HT): Involved in satiety, mood regulation, impulse control, and anxiety
- AN patients: altered 5-HT function — starvation reduces tryptophan (5-HT precursor) availability, but post-recovery 5-HT levels may actually be elevated, suggesting an underlying trait of heightened 5-HT activity that produces anxiety/obsessionality. Starvation may be an unconscious attempt to reduce this aversive state ^[2]
- BN patients: 5-HT dysfunction similar to that seen in depression and impulsivity disorders ^[2]
Dopamine (DA): Involved in reward processing
- AN patients: altered DA reward signalling — food may not generate normal reward signals, and patients may derive reward from self-denial instead
- BN patients: DA abnormalities similar to addictive patterns — binge eating may temporarily activate DA reward pathways ^[2]

The Serotonin Starvation Hypothesis

Think of it this way: some individuals are born with overactive serotonin systems → they feel chronically anxious, perfectionistic, obsessional. Starvation reduces tryptophan → reduces serotonin → temporarily reduces anxiety. So starvation becomes self-reinforcing because it makes the patient feel calmer. This is why AN patients often describe feeling "better" when restricting — they are literally self-medicating their anxiety through caloric restriction. Recovery then feels aversive because serotonin function normalises and anxiety returns.

Hormone	Normal function	Change in AN	Consequence
Leptin (from adipose tissue)	Signals satiety; suppresses appetite	↓↓ (due to ↓ fat mass)	↓ Satiety signalling; drives hunger (which patients override cognitively)
Ghrelin (from stomach)	Stimulates appetite ("hunger hormone")	↑↑	Should increase appetite, but patients cognitively override this drive
Peptide YY	Signals satiety post-meal	↑ (paradoxically) in some AN patients	May contribute to early satiety complaints
Insulin	Anabolic; promotes glucose uptake	↓ (due to chronic caloric restriction)	Hypoglycaemia
Growth hormone	Growth and metabolism	↑ (GH resistance in starvation)	↓ IGF-1 → poor growth in pre-pubertal patients

Insula: Processes interoceptive signals (hunger, fullness, disgust). Altered insular function in AN → poor recognition of hunger/satiety cues
Prefrontal cortex: Cognitive control; in AN, excessive top-down cognitive control overrides normal appetitive drives
Ventral striatum: Reward processing; altered in both AN (reduced food reward) and BN/BED (heightened food reward, reduced satiety)

5. Aetiology

Eating disorders result from gene-environment interactions — a complex interplay of biological vulnerability, psychological factors, family dynamics, and sociocultural pressures ^[2].

5.1 Biological Factors

Eating disorders are highly heritable: 50–80% genetic influence ^[2]
Family studies: ~12× risk for first-degree relatives of AN patients ^[2]
Twin studies: MZ concordance rate = 55% vs DZ = 24% ^[2]
Mode of inheritance: No single gene identified for AN; risk is transmitted via:
- Temperamental traits (anxiety, perfectionism, obsessionality)
- Shared heritability with OCD, schizophrenia, depression, and anxiety disorders ^[2]
- Genome-wide association studies (GWAS) have identified loci on chromosomes 1 and 12, with overlap with metabolic traits (BMI, insulin resistance) — suggesting AN has both psychiatric AND metabolic genetic components

5-HT dysfunction and DA abnormalities (as detailed above) ^[2]
Negative affect due to imbalance between aversive (5-HT) and reward (DA) systems → pathological eating as a maladaptive attempt to resolve this affect ^[2]

AN traits: Harm-avoidant, neurotic, obsessional, anxious, perfectionistic, reward-dependent, low novelty-seeking, extreme ↓ self-esteem, less affective dysregulation, less impulsivity ^[2]
BN traits: Also harm-avoidant, neurotic, anxious, perfectionistic — but MORE impulsive, may exhibit borderline personality traits, greater affective dysregulation ^[2]

The personality profile tells you something about the neurobiology: AN patients have excessive cognitive control (prefrontal dominance), while BN patients have impaired impulse control (limbic/striatal dominance relative to prefrontal cortex).

5.2 Psychological Factors

Premorbid personality traits (anxious, perfectionistic) → difficulty negotiating demands of adolescence → pathological eating as a maladaptive attempt to struggle for control, sense of identity, and effectiveness ^[2]
Pathological eating → neurobiological changes → ↑ negative affect → vicious cycle ^[2]
Think of the developmental trajectory:
- Childhood: mild anxiety, perfectionism, obsessionality
- Adolescence: puberty + brain development + stress + cultural pressures → neurobiological change
- Vicious cycle: increased dysphoria, denial, perfectionism, obsessionality → either poor outcome (chronic) or good outcome (recovered) if the cycle is broken ^[2]

Childhood adversities: Poor relationship with parents, parental psychiatric disorder, history of anxiety or depression, sexual or physical abuse ^[2]
Developmental risk factors: Early onset puberty, prior elevated BMI, weight loss from physical illness ^[2]
Other personal factors: Poor problem-solving skills, impulsivity (especially BN), fears about sexuality ^[2]

FHx of psychiatric illness: Depression, alcoholism, eating disorder, substance abuse ^[2]
Disturbed family relationships: Enmeshment, overprotectiveness, rigidity, lack of conflict resolution → development of AN may serve to "prevent dissent within family" ^[2]
Poor parenting: Parental deprivation, sexual abuse, physical abuse, emotional abuse ^[2]

General: Dieting culture, social pressure on women, emphasis on thinness, role confusion, mixed messages on women ^[2]
Specific: Typically in highly competitive academic or social environments ^[2]
Important nuance for AN: AN patients typically have no excess exposure to factors associated with dieting — the problem is how the individual reacts to dieting rather than dieting itself ^[2]

While sharing many risk factors with AN, BN has additional/distinct risk factors ^[2]:

General RFs for psychiatric disorders: General genetic risk genes, FHx of depression, substance abuse, childhood adverse experiences (e.g., sexual abuse)
RFs for dieting: ↑ exposure to factors promoting dieting, e.g., childhood/parental obesity, early menarche
Personal RFs: Premorbid negative self-evaluation, parental problems (low contact, high expectations)

Immediate precipitating factors are almost always internal/external experiences of feeling out of control ^[2]:

Onset of puberty (11–14 years): Average gain of ~40 lbs with disproportionate fat ratio → body changes feel "out of control"
Life events: Major life transitions, traumatic events, family difficulties
Onset of comorbid illness: e.g., anxiety or depression
Weight loss through dieting and/or exercise (the "gateway")

The 'Dieting Gets Out of Control' Narrative

The typical natural history of AN begins with an ordinary effort at dieting in adolescence. Then:

Dieting gets out of control: secrecy and lying about eating, continued weight loss after overshooting target, preserved hunger
AN "takes over": extreme fear of weight gain, total preoccupation with food and weight, loss of hunger, metabolism stabilises making further weight loss harder
Symptoms of starvation: cold intolerance, hypoglycaemia, dizziness, fatigue, anergia...

Understanding this trajectory helps you recognise early presentations before the illness becomes entrenched ^[2].

6. Pathophysiology of Physical Complications

This section explains why each physical complication occurs — connecting clinical features back to the underlying pathophysiology of starvation, purging, and metabolic derangement.

System	Pathophysiology	Consequence
Endocrine	Chronic energy deficit → ↓ leptin → hypothalamic suppression of GnRH → ↓ LH/FSH	Amenorrhoea (F), ↓ libido/impotence (M) ^[2]
Endocrine	Chronic stress → ↑ CRH → ↑ ACTH → ↑ cortisol; dexamethasone non-suppression	Pseudo-Cushing's; contributes to osteoporosis, mood disturbance ^[2]
Endocrine	Starvation → ↓ T3 (euthyroid sick syndrome); GH resistance → ↑ GH but ↓ IGF-1	Cold intolerance, bradycardia, dry skin; growth retardation in children ^[2]
Endocrine	↓ Insulin secretion in chronic caloric restriction	Hypoglycaemia ^[2]
Metabolic	Starvation → lipolysis → ↑ free fatty acids → hepatic cholesterol synthesis	Hypercholesterolaemia (paradoxical — patients are malnourished but have high cholesterol!) ^[2]
Metabolic	↑ Dietary carotene relative to metabolic clearance (or ↑ intake of low-calorie carotenoid-rich vegetables)	Raised serum carotene → yellowish skin (carotenodermia) ^[2]
Metabolic	Intracellular phosphate depletion during chronic starvation; worsened during refeeding (see below)	Hypophosphataemia ^[2]
Cardiovascular	Chronic caloric restriction → ↓ cardiac muscle mass → ↓ cardiac output; vagal predominance	Bradycardia, hypotension, peripheral cyanosis
Cardiovascular	Electrolyte disturbances (especially ↓ K⁺, ↓ Mg²⁺) → altered cardiac repolarisation	QT prolongation → risk of arrhythmia and sudden cardiac death ^[2]
Haematological	Starvation → gelatinous bone marrow transformation (fat replaced by mucopolysaccharide) → ↓ haematopoiesis	Normocytic normochromic anaemia, mild leucopenia with relative lymphocytosis, thrombocytopenia ^[2]
Skeletal	↓ Oestrogen + ↑ cortisol + ↓ IGF-1 + ↓ calcium/vitamin D intake → impaired osteoblast function, enhanced osteoclast activity	Osteopenia and osteoporosis (can be irreversible) ^[2]
GI	↓ Autonomic tone + ↓ gut hormones → impaired gastric motility	Delayed gastric emptying → bloating, early satiety (reinforces restriction) ^[2]
GI	Chronic laxative misuse → damage to myenteric plexus	Decreased colonic motility, chronic constipation ^[2]
GI	Rapid, excessive refeeding or binge eating → gastric atony	Acute gastric dilatation (rare but potentially fatal) ^[2]
Dermatological	Starvation → hypothermia → compensatory lanugo hair growth	Lanugo — fine, downy hair on face, arms, trunk
Neurological	Starvation → cerebral atrophy (grey and white matter volume loss)	Cognitive impairment, ↓ concentration (partially reversible with refeeding)
Renal	Dehydration + ↓ GFR + electrolyte disturbances	Pre-renal AKI, electrolyte derangements

Purging method	Pathophysiology	Consequence
Self-induced vomiting	Loss of H⁺ and Cl⁻ in gastric acid → metabolic alkalosis with hypokalaemia (renal K⁺ wasting to compensate) and hypochloraemia	Electrolyte disturbances, cardiac arrhythmia ^[2]
Self-induced vomiting	Repeated exposure of teeth to gastric acid → dissolution of dental enamel	Dental erosion (perimolysis) — especially palatal surfaces of upper teeth ^[2]
Self-induced vomiting	Chronic parotid stimulation from repeated vomiting → sialadenosis (non-inflammatory parotid hypertrophy)	Parotid enlargement (bilateral, painless) ^[2]
Self-induced vomiting	Forceful retching → mucosal tear at gastro-oesophageal junction	Mallory-Weiss tear → haematemesis ^[2]
Self-induced vomiting	↑ Intra-abdominal pressure → rupture of small vessels	Epistaxis, subconjunctival haemorrhage ^[2]
Self-induced vomiting	Chronic acid exposure to oesophageal mucosa	GERD, oesophagitis, Barrett's oesophagus (long-term) ^[2]
Self-induced vomiting	Dorsal hand repeatedly hitting upper teeth during gag reflex	Russell's sign — calluses/scarring on dorsum of hand
Laxative misuse (stimulant)	Stimulant laxatives → ↑ colonic water and electrolyte secretion → loss of Na⁺, K⁺, and HCO₃⁻	HypoNa⁺, hypoK⁺, metabolic acidosis ^[2]
Laxative misuse (stimulant)	Chronic stimulant laxative use → lipofuscin deposition in colonic mucosa	Melanosis coli ^[2]
Laxative misuse (stimulant)	Damage to myenteric plexus ("cathartic colon")	Chronic constipation (paradoxically worsened) ^[2]
Diuretic misuse	↑ Renal excretion of Na⁺, K⁺, water	Dehydration, hypoNa⁺, hypoK⁺

Vomiting = Alkalosis, Laxatives = Acidosis

A common exam trap: self-induced vomiting causes metabolic alkalosis (loss of gastric HCl), while stimulant laxative misuse causes metabolic acidosis (loss of bicarbonate-rich intestinal secretions). If you see a purging patient with acidosis, think laxatives; if alkalosis, think vomiting ^[2].

7. Clinical Features

7.1 Anorexia Nervosa — Symptoms

Every symptom can be traced back to either (a) the core psychopathology, (b) starvation, or (c) compensatory behaviours.

Symptom	Pathophysiological Basis
Intense fear of gaining weight / becoming fat	Core over-evaluation of weight and shape; maintained by cognitive distortions (black-and-white thinking, catastrophising about weight gain) ^[2]
Strong desire to become thin	Ego-syntonic belief that thinness = worth, control, identity ^[2]
Disturbance in body image — feeling "fat" despite being objectively underweight	Perceptual distortion (altered body representation in parietal cortex and insula) + cognitive bias (selective attention to perceived "fat" areas) ^[2]
Persistent lack of recognition of seriousness of low body weight (poor insight/anosognosia)	Ego-syntonic nature of AN; cognitive rigidity; possibly related to altered interoception (impaired insular function) ^[2]
Undue influence of body weight/shape on self-evaluation	The defining cognitive distortion — self-worth = weight/shape control ^[2]
Preoccupation with food — cooking elaborate meals for others, collecting recipes, hoarding food	Starvation itself drives obsessive thoughts about food (demonstrated in Keys' Minnesota Starvation Experiment); paradoxical food-related behaviours reflect both cognitive preoccupation and possible vicarious satisfaction ^[2]

Symptom	Pathophysiological Basis
Amenorrhoea (females) / ↓ libido, impotence (males)	HPG axis suppression (↓ GnRH pulsatility → ↓ LH/FSH → ↓ oestrogen/testosterone) secondary to energy deficit. Occurs early in the illness — often before dramatic weight loss ^[2]
Cold intolerance	↓ Basal metabolic rate + ↓ subcutaneous fat insulation + hypothyroidism (sick euthyroid syndrome: ↓ T3)
Fatigue, anergia, weakness	Chronic caloric deficit → ↓ glycogen stores → ↓ available ATP; also muscle wasting
Dizziness, lightheadedness	Orthostatic hypotension (↓ cardiac output + ↓ intravascular volume) + hypoglycaemia ^[2]
Constipation	↓ Colonic motility (↓ autonomic tone + ↓ food volume to stimulate peristalsis); worsened by chronic laxative misuse ^[2]
Bloating, early satiety	Delayed gastric emptying (gastroparesis of starvation) ^[2]
Depression, anxiety, irritability, labile mood	Multifactorial: 5-HT/DA dysfunction from starvation, social isolation, chronic stress, hypercortisolaemia ^[2]
Obsessional symptoms (about food, weight, exercise, rituals)	Starvation amplifies pre-existing obsessional traits; 5-HT dysfunction
Social withdrawal	Combination of depression, food-related anxiety in social situations, and ego-syntonic avoidance
↓ Concentration, cognitive impairment	Cerebral atrophy from starvation + hypoglycaemia + electrolyte disturbance
Insomnia	Hypercortisolaemia + hunger + anxiety

Symptom	Mechanism
Self-induced weight loss by limiting energy intake (often 600–1000 kcal/day)	Deliberate caloric restriction driven by core psychopathology ^[2]
Purging behaviour: self-induced vomiting, misuse of laxatives/diuretics/enemas	Compensatory behaviour to "undo" perceived caloric intake ^[2]
Excessive exercising	Compulsive caloric expenditure; often ritualistic and distressing if prevented
Binge eating (in binge-eating/purging subtype)	Increases in frequency with chronicity and age; typical binge involves eating "forbidden" foods → intense guilt → compensatory purging ^[2]
Food-related rituals (cutting food into tiny pieces, eating very slowly, sorting foods)	Attempt to exert control; starvation-driven obsessionality
Deliberate self-harm	22% lifetime risk; reflects comorbid depression, impulsivity, and emotional dysregulation ^[2]

7.2 Anorexia Nervosa — Signs

Sign	Pathophysiological Basis
Abnormally low body weight: BMI ≤ 17.5 kg/m² or ≥ 15% below expected weight; in children, failure to gain weight or grow	Chronic caloric deficit — the hallmark finding ^[2]
Emaciated, cachectic appearance	Severe muscle wasting + ↓ subcutaneous fat
Lanugo hair (fine, downy hair on face, arms, trunk)	Compensatory mechanism for hypothermia: the body grows fine hair to trap an insulating layer of warm air near the skin (similar to goosebumps)
Dry, yellowish skin (carotenodermia)	↑ Serum carotene (from ↑ relative carotene intake in vegetable-heavy diets and ↓ metabolic clearance) ^[2]
Hair thinning/alopecia	Protein malnutrition → telogen effluvium (hair follicles shift prematurely to resting phase)
Peripheral oedema	Hypoalbuminaemia from malnutrition → ↓ oncotic pressure

Sign	Pathophysiological Basis
Bradycardia (HR < 60 bpm, often < 40)	↓ Metabolic demand → compensatory ↑ vagal tone; ↓ cardiac muscle mass
Hypotension, postural hypotension	↓ Intravascular volume + ↓ cardiac output + ↓ autonomic response
Peripheral cyanosis, cold extremities	↓ Cardiac output → peripheral vasoconstriction to preserve core temperature
Cardiac arrhythmias	Electrolyte disturbances (hypoK⁺, hypoMg²⁺) → QT prolongation → risk of torsades de pointes / VF ^[2]

Sign	Basis
Abdominal distension	Gastroparesis + constipation + possible acute gastric dilatation
↓ Bowel sounds	↓ Colonic motility

Sign	Basis
Proximal myopathy	Protein catabolism → skeletal muscle wasting
Pathological fractures	Osteoporosis from ↓ oestrogen + ↑ cortisol + ↓ calcium/vitamin D + ↓ IGF-1 ^[2]

Sign	Basis
↓ Deep tendon reflexes	Electrolyte disturbance (hypoK⁺) + peripheral neuropathy from malnutrition
Peripheral neuropathy	Vitamin deficiency (B1, B6, B12)

Sign	Basis
Russell's sign — calluses/scarring on dorsum of hand	Repeated trauma from teeth during self-induced vomiting
Parotid/salivary gland enlargement (bilateral, painless)	Sialadenosis from chronic vomiting-induced stimulation ^[2]
Dental erosion (perimolysis) — especially palatal surfaces	Repeated acid exposure from gastric contents ^[2]
Pharyngeal erythema	Chemical irritation from repeated vomiting

7.3 Bulimia Nervosa — Symptoms

BN is characterised by a prototypic cyclic binging-purging behaviour ^[2]:

Morbid dread of fatness with strict weight threshold — the same core over-evaluation of weight and shape as AN ^[2]
Irresistible craving for food → episodes of binge eating ^[2]
May have a history of AN (30%) ^[2]

Recurrent episodes of excessive eating of large amounts of food ^[2]
Associated with a sense of loss of control during the episode — the patient feels they "cannot stop eating or control what or how much they are eating" ^[2]
Precipitated by: Stress, breaking of self-imposed dietary rules (the "abstinence violation effect" — one bite of "forbidden food" → catastrophic thinking → "I've already blown it" → full binge) ^[2]
Consequence: Initially feel relief from tension → soon followed by guilt and disgust → drives compensatory behaviour ^[2]

Purging: Self-induced vomiting, laxative/diuretic/appetite suppressant use ^[2]
Non-purging: Fasting, excessive exercise ^[2]

This cycle is self-perpetuating ^[2]:

Strict dieting → physiological and psychological tension/hunger
Craving builds until the patient succumbs
Binge eating → temporary relief from tension
Shame and disgust → compensatory purging
Purging → renewed strict dieting → back to step 1

Depression — very common; typically remits when BN is treated (suggesting it is secondary to the eating disorder rather than a primary comorbidity) ^[2]
Impulsivity — may manifest as substance misuse, shoplifting, sexual disinhibition
Self-harm

Body weight is often normal or near-normal — this is the key distinguishing feature from AN. Patients with BN may be slightly underweight, normal weight, or even overweight.
Parotid enlargement (sialadenosis) — bilateral, painless ^[2]
Dental erosion (perimolysis) — especially palatal surfaces of upper incisors ^[2]
Russell's sign — calluses/scarring on dorsum of hand ^[2]
Subconjunctival haemorrhage, epistaxis — from forceful retching (↑ venous pressure) ^[2]
Metabolic alkalosis (from vomiting) or metabolic acidosis (from laxative abuse) ^[2]
Electrolyte disturbances: HypoK⁺ (most dangerous — can cause fatal arrhythmia), hypoNa⁺, hypoCl⁻ ^[2]
Mallory-Weiss tear — presents as haematemesis after forceful retching ^[2]
GERD symptoms — heartburn, oesophagitis ^[2]
Melanosis coli — brownish discolouration of colonic mucosa from chronic stimulant laxative use ^[2]

Recurrent episodes of binge eating (same definition as in BN: large amounts of food in a discrete period, with loss of control)
WITHOUT recurrent inappropriate compensatory behaviours — this is the critical distinction from BN
Associated features during binge episodes:
- Eating much more rapidly than normal
- Eating until uncomfortably full
- Eating large amounts when not physically hungry
- Eating alone due to embarrassment
- Feeling disgusted, depressed, or very guilty afterward
Marked distress regarding binge eating
Frequency: At least once per week for 3 months (DSM-5)
Patients are often overweight or obese but not all obese patients have BED

Not driven by body image concerns — this is the key distinction from AN
Instead, restriction is driven by:
- Sensory sensitivity (texture, colour, smell of food)
- Fear of aversive consequences (e.g., choking, vomiting)
- Apparent lack of interest in eating or food
Can present at any age (including young children)
Can lead to significant nutritional deficiency, weight loss, growth failure

AN vs ARFID — The Body Image Test

Both AN and ARFID present with low weight and food restriction. The differentiator is the motivation: AN patients restrict because of over-evaluation of weight/shape and fear of fatness. ARFID patients restrict for entirely different reasons (sensory aversion, fear of choking, lack of appetite) with no body image distortion. This is a common exam distinction.

8. Approach to Assessment

Patients with eating disorders are often ambivalent or reluctant about seeking help — the illness is often ego-syntonic (especially AN). An empathic, non-judgmental approach is essential ^[2].

Domain	Key Questions
Eating History	Typical day of eating? Mealtime arrangements? Any hunger? What foods are avoided and why? Calorie counting? Food rituals? ^[2]
Weight and Shape Concerns	How do you feel about your weight/shape? What would happen if you gained 1–2 kg? How often do you weigh yourself?
Compensatory Behaviours	Self-induced vomiting? Laxative/diuretic use? Excessive exercise? Fasting?
Binge Eating	Episodes of eating large amounts? Sense of loss of control? Frequency? Triggers?
Weight History	Highest/lowest weight? Rate of weight loss? Growth chart (children)?
Menstrual History	Regular periods? Amenorrhoea? Age at menarche?
Psychiatric Comorbidities	Depression? Anxiety? OCD? Self-harm? Suicidal ideation? Substance use?
Past History	Previous eating disorder episodes? Previous treatment? Medical complications?
Family History	FHx of eating disorders, depression, alcoholism, substance abuse?
Developmental/Social History	Childhood adversities? Sexual/physical abuse? Family dynamics? Academic/social pressures?

Vitals: Weight, height, BMI, heart rate (look for bradycardia), blood pressure (look for orthostatic hypotension), temperature (hypothermia)
General: Cachexia, lanugo, dry skin, carotenodermia, peripheral oedema, hair thinning
Oral cavity: Dental erosion, parotid enlargement, pharyngeal erythema
Hands: Russell's sign, peripheral cyanosis
Cardiovascular: Bradycardia, arrhythmia, hypotension
Abdominal: Distension, ↓ bowel sounds
Musculoskeletal: Proximal myopathy, tenderness over bones (fractures)

Investigation	Purpose
FBC	Anaemia, leucopenia, thrombocytopenia (bone marrow suppression) ^[2]
UEC (Urea, electrolytes, creatinine)	HypoK⁺, hypoNa⁺ (most critical — life-threatening arrhythmia risk) ^[2]
Calcium, magnesium, phosphate	Hypophosphataemia (especially during refeeding), hypoMg²⁺ ^[2]
Glucose	Hypoglycaemia ^[2]
LFTs	Transaminitis (starvation-related hepatocellular damage, or refeeding)
TFTs	↓ T3, normal/low TSH (sick euthyroid syndrome)
Lipid profile	Hypercholesterolaemia ^[2]
Serum amylase	↑ (salivary amylase from parotid hypertrophy) — marker of vomiting
Bone densitometry (DEXA scan)	Osteopenia/osteoporosis ^[2]
ECG	Bradycardia, QT prolongation, U waves (hypoK⁺), arrhythmias ^[2]
Urinalysis	Specific gravity (dehydration), pH (metabolic alkalosis vs acidosis)
Oestradiol / Testosterone, LH, FSH	Hypogonadism ^[2]

9. Course and Prognosis

Onset: Usually begins in adolescence following an ordinary effort at dieting ^[2]
1. Dieting gets out of control: secrecy, lying, continued weight loss after overshooting target, preserved hunger
2. AN "takes over": extreme fear of weight gain, total preoccupation with food/weight, loss of hunger, harder to lose weight as metabolism stabilises
3. Symptoms of starvation: cold intolerance, hypoglycaemia, dizziness, fatigue, anergia ^[2]
Course: Generally fluctuating with exacerbations and periods of partial remission ^[2]
Prognosis: Earlier treatment (< 15 years old) → better outcomes ^[2]
- Adolescents: Excellent outcomes with family-based treatment → 60% well at 1 year, 90% well at 5 years ^[2]
- Adults: Different psychotherapy (mainly individual) better than specialist or dietary treatment alone → 30% well at 1 year, 40–50% well at 5 years ^[2]
Poor prognostic factors: Onset before puberty or in adulthood, long history ( > 3 years), premorbid personality problems, comorbid substance abuse, childhood obesity, shorter duration of maintaining normal BMI ^[2]

Prognosis: Generally better than AN
~50% recover fully; ~30% have partial recovery; ~20% have chronic course
Relapse is common, particularly in the first 2 years after treatment

Feature	AN	BN	BED
Weight	Significantly low (BMI ≤ 17.5)	Normal or near-normal	Often overweight/obese
Core psychopathology	Over-evaluation of weight/shape	Over-evaluation of weight/shape	Distress about binge eating
Restriction	Prominent	Present (between binges)	Not prominent
Binge eating	May be present (subtype)	Always present	Always present
Compensatory behaviours	May be present (subtype)	Always present	Absent
Insight	Often poor (ego-syntonic)	Usually better (ego-dystonic)	Variable
Key metabolic risk	Starvation, refeeding syndrome	Electrolyte disturbance from purging	Metabolic syndrome
Mortality	Highest of all psychiatric disorders	Lower than AN	Related to obesity complications
Personality traits	Rigid, perfectionistic, controlled	Impulsive, affectively dysregulated	Variable

High Yield Summary

Core psychopathology of all eating disorders: over-evaluation of weight and shape — self-worth = ability to control weight/shape/eating.
AN epidemiology: 3rd commonest chronic illness in teenage girls; F:M = 10:1; onset around menarche; highest mortality of ALL psychiatric disorders (SMR 23.14×); death from suicide (32%), starvation (19%), cancer (11%).
AN is ego-syntonic → poor insight; BN is ego-dystonic → better insight.
Aetiology = gene-environment interaction: 50–80% heritable; 12× risk in first-degree relatives; transmitted via temperamental traits (anxiety, perfectionism); precipitated by feeling "out of control" (puberty, life events).
Starvation physiology: HPG axis suppression → amenorrhoea; HPA activation → ↑ cortisol; ↓ T3 (sick euthyroid); bradycardia, hypotension, hypothermia; osteoporosis (↓ oestrogen + ↑ cortisol); gelatinous marrow → pancytopenia; hypercholesterolaemia (paradoxical); hypoglycaemia.
Purging: vomiting → metabolic alkalosis + hypoK⁺; laxatives → metabolic acidosis + hypoK⁺/Na⁺ — common exam trap!
BN vicious cycle: Strict diet → tension → craving → binge → guilt/disgust → purging → strict diet → repeat.
AN vs ARFID: Both have low weight + restriction. AN = fear of fatness/body image distortion. ARFID = no body image concern (sensory aversion, fear of choking, lack of interest).
Severity specifiers: AN = by BMI (mild ≥ 17, extreme < 15); BN = by compensatory behaviour frequency/week (mild 1–3, extreme ≥ 14).
Prognosis: Earlier treatment → better outcome. Adolescent AN with family-based treatment: 90% well at 5 years. Poor prognostic factors: late onset, long duration, personality problems, substance abuse.

Active Recall - Eating Disorders (Definition through Clinical Features)

^[1] Lecture slides: GC 167. I feel very nervous Anxiety disorders.pdf (general psychiatric context) ^[2] Senior notes: ryanho-psych.md (Sections 9.1, 9.1.1 — Eating Disorders, Anorexia Nervosa, Bulimia Nervosa)

Differential Diagnosis of Eating Disorders

The differential diagnosis of eating disorders is crucial because significant weight loss, abnormal eating patterns, and associated physical findings can be caused by a wide range of medical and psychiatric conditions. The clinical challenge is to distinguish primary eating disorders (where the psychopathology drives the weight/eating disturbance) from conditions where weight loss or abnormal eating is secondary to another process.

The golden rule: does the patient have the core psychopathology of over-evaluation of weight and shape? If yes → primary eating disorder. If no → look harder for an alternative diagnosis ^[2].

These are conditions that cause weight loss, poor appetite, or GI symptoms that can mimic an eating disorder — but the psychopathology of body image distortion and fear of fatness is absent.

Why is the medical differential important?

Because medical conditions can cause exactly the same physical findings (cachexia, amenorrhoea, electrolyte disturbances, bradycardia) as AN. If you don't exclude them, you may miss a treatable — or life-threatening — organic disease. Equally, some medical conditions can coexist with an eating disorder (e.g., a patient with coeliac disease who also develops AN), making diagnosis more complex.

Medical Condition	Why It Can Mimic AN/Eating Disorders	Key Differentiating Features
Neoplasia (e.g., GI tumours, hypothalamic tumours, lymphoma, cachexia from any malignancy) ^[2]	Malignancy causes weight loss through increased metabolic demand, cytokine-mediated cachexia (TNF-α, IL-6), mechanical obstruction, or hypothalamic dysfunction disrupting appetite centres	No fear of fatness or body image distortion. Patient typically wants to eat but cannot. Hypothalamic tumours are particularly treacherous — they can directly impair appetite regulation while also causing endocrine dysfunction (hypopituitarism) that mimics AN. Look for: focal neurological signs, visual field defects (bitemporal hemianopia from optic chiasm compression), other pituitary hormone deficiencies, B symptoms (fever, night sweats, weight loss) for lymphoma
Inflammatory Bowel Disease (Crohn's disease, ulcerative colitis) ^[2]	Chronic inflammation → malabsorption, increased metabolic demand, abdominal pain limiting intake, corticosteroid-related complications	Abdominal pain, bloody diarrhoea, perianal disease (Crohn's), raised inflammatory markers (CRP, ESR), anaemia of chronic disease. No body image distortion. However, be aware that adolescents with IBD can develop secondary eating avoidance that evolves into a true eating disorder
Malabsorption syndromes (e.g., coeliac disease, chronic pancreatitis) ^[2]	Impaired nutrient absorption despite adequate intake → weight loss, nutritional deficiencies, GI symptoms (bloating, diarrhoea, steatorrhoea)	Coeliac: positive anti-tTG/anti-endomysial antibodies, villous atrophy on duodenal biopsy, iron/folate deficiency, dermatitis herpetiformis. Chronic pancreatitis: history of alcohol use or gallstones, steatorrhoea, epigastric pain radiating to back, pancreatic calcifications on imaging. No over-evaluation of weight/shape
Hyperthyroidism ^[2]	↑ Metabolic rate → weight loss despite normal or increased appetite; also causes anxiety, tremor, heat intolerance, diarrhoea, tachycardia	Key distinction from AN: patients with hyperthyroidism typically have increased appetite (eating more but losing weight), tachycardia (AN has bradycardia), heat intolerance (AN has cold intolerance), tremor, lid lag, goitre. TFTs: ↓ TSH, ↑ free T4/T3
Diabetes mellitus ^[2]	Type 1 DM: Insulin deficiency → inability to utilise glucose → weight loss, polyuria, polydipsia, polyphagia. "Diabulimia": Deliberate insulin omission for weight control — a dangerous overlap where true eating disorder psychopathology coexists with DM	Type 1 DM: Hyperglycaemia, ketoacidosis, polyuria, polydipsia. Diabulimia is particularly important — patients with T1DM may deliberately withhold insulin to induce glycosuria and weight loss; this carries an extremely high mortality. Look for: recurrent DKA, persistently elevated HbA1c despite apparent adherence, early microvascular complications
Pituitary failure (hypopituitarism) ^[2]	Panhypopituitarism → ↓ ACTH, TSH, GH, gonadotropins → weight loss, fatigue, amenorrhoea, hypotension — closely mimics AN	Shared features with AN: amenorrhoea, low gonadotropins, fatigue, hypotension. Differentiators: ↓ cortisol (AN has ↑ cortisol), ↓ TSH with ↓ T4 (AN has normal TSH with ↓ T3), visual field defects if pituitary adenoma, headache. No body image distortion. Must measure cortisol, TSH, free T4, IGF-1
Chronic infection (e.g., TB, HIV, chronic hepatitis) ^[2]	Chronic immune activation → cytokine-mediated cachexia, malabsorption, anorexia	Fever, night sweats, lymphadenopathy, specific organ involvement. Travel/exposure history. HIV testing. TB screening (CXR, sputum, IGRA). No body image distortion
Cystic fibrosis ^[2]	Pancreatic insufficiency → malabsorption + ↑ metabolic demand from chronic respiratory infection → failure to thrive and weight loss	Chronic productive cough, recurrent chest infections, clubbing, steatorrhoea. Usually diagnosed in childhood but mild phenotypes may present in adolescence
Addison's disease (primary adrenal insufficiency)	↓ Cortisol → anorexia, nausea, weight loss, fatigue, hypotension, hyperpigmentation	Hyperpigmentation (ACTH-driven, especially in palmar creases, buccal mucosa), hyperkalaemia + hyponatraemia (opposite to AN which has hypoK⁺), postural hypotension. Confirm with short Synacthen test

Hypothalamic Tumours — The Great Mimicker

Hypothalamic tumours (e.g., craniopharyngioma in adolescents) are a particularly dangerous mimic of AN. They can cause: weight loss, amenorrhoea, growth failure, behavioural changes, and even apparent food refusal. The difference is that there is no over-evaluation of weight/shape — the appetite disturbance is neurological, not psychological. Always consider a brain MRI in atypical presentations (e.g., male patients, very young patients, patients without typical body image distortion, or patients with headache/visual symptoms) ^[2].

These are psychiatric conditions where abnormal eating, weight loss, or body-related preoccupation occurs — but the specific eating disorder psychopathology either differs or is absent.

Psychiatric Condition	Why It Can Mimic Eating Disorders	Key Differentiating Features
Bulimia Nervosa (vs AN) ^[2]	Both AN and BN share over-evaluation of body shape and weight; some AN patients exhibit binge eating and purging behaviour as in BN	The key distinguishing feature is body weight: AN requires an abnormally low body weight, often associated with structural and physiological sequelae. BN patients are typically at normal or near-normal weight. If a patient is severely underweight AND binge-purging, they have AN binge-eating/purging subtype, NOT BN ^[2]
ARFID (Avoidant/Restrictive Food Intake Disorder) ^[2]	Also associated with poor energy and nutritional intake leading to low body weight	Due to a lack of interest in food, aversion to sensory characteristics, or concern about aversive consequences of eating (e.g., fear of choking, vomiting) — NOT due to fear of fatness or body image distortion. No over-evaluation of weight/shape ^[2]
OSFED / Atypical Eating Disorders ^[2]	Patients exhibit features of AN/BN but both diagnostic criteria for AN and BN cannot be fully met	Examples: atypical AN (all criteria for AN met except weight is within/above normal range despite significant weight loss), subthreshold BN (binge/purge frequency < 1/week), purging disorder (purging without binge eating), night eating syndrome ^[2]
Depression ^[2]	Depressive disorder commonly causes ↓ appetite and weight loss (neurovegetative symptoms); can also cause ↑ appetite in atypical depression	Weight loss in depression is secondary to anhedonia and ↓ appetite — the patient does not fear weight gain and does not have body image distortion. They are typically distressed by weight loss, not gratified by it. Also look for: pervasive low mood, anhedonia, guilt, hopelessness, sleep disturbance, suicidal ideation. Caveat: Depression frequently coexists with eating disorders (75% lifetime comorbidity in AN) — the question is which is primary ^[2]
OCD ^[2]	Both AN and OCD may have obsessional thoughts and ritualistic behaviours (food rituals, body checking, exercise rituals)	In OCD, obsessions are ego-dystonic (the patient recognises them as intrusive, unwanted, and distressing) and are not specifically focused on weight and shape. In AN, the preoccupation with weight/shape is ego-syntonic (feels "right" and aligned with the patient's values). OCD obsessions are diverse in content (contamination, harm, symmetry), while AN obsessions are narrowly focused on food/weight/shape. However: OCD is highly comorbid with AN, so look carefully at whether the eating-related preoccupations are the patient's only obsessions or part of a broader OCD pattern ^[2]
Social Anxiety Disorder ^[2]	Patients may feel ashamed to be seen eating in public → avoidance of eating in social situations → weight loss	Patients usually recognise that the fear is excessive and unreasonable. The core fear is about social evaluation in general (embarrassment, humiliation), not specifically about weight or shape. They eat normally in private. No compensatory behaviours or binge eating ^[2]
Body Dysmorphic Disorder (BDD) ^[3]	Preoccupation with perceived defects in physical appearance → distress, compulsive behaviours (mirror checking, camouflaging, skin picking), social avoidance	BDD preoccupation is with a specific body part (skin, nose, hair — not overall body weight/shape). Patients believe they look "ugly" or "deformed," not "fat." BDD patients do not restrict food intake to change the perceived defect. However: BDD and eating disorders frequently co-occur (~33% comorbidity), and some patients have both weight/shape concerns AND appearance concerns about specific features. The focus of preoccupation is the differentiator ^[3]
Somatoform / Somatic Symptom Disorder ^[2]	May present with GI complaints (nausea, abdominal pain, vomiting) that limit food intake → weight loss	No over-evaluation of weight/shape. The patient's concern is about physical symptoms, not body image. Weight loss is a consequence of symptom burden, not a goal. Look for: multiple somatic complaints, excessive health anxiety, extensive negative investigations
Psychotic Disorders (e.g., schizophrenia) ^[4]	Patients may refuse food due to paranoid delusions (e.g., food is poisoned), command auditory hallucinations (voices telling them not to eat), or disorganisation	Food refusal in psychosis is driven by delusional beliefs or hallucinations, not by fear of fatness. Note the theme of the anxiety — "worry about being poisoned" points to paranoid schizophrenia, not AN. Also look for: formal thought disorder, negative symptoms, bizarre behaviour. However: psychotic symptoms can rarely occur in severe AN (usually at very low BMI), so always assess whether psychotic features are primary or secondary to starvation ^[2]^[4]
Substance Use Disorders	Stimulants (amphetamines, cocaine, methamphetamine) → appetite suppression → weight loss; alcohol use disorder can cause malnutrition	Weight loss is secondary to substance effects, not body image concerns. Drug history is essential. Look for: dilated pupils, nasal septal perforation (cocaine), injection marks, erratic behaviour. However: substance misuse can coexist with eating disorders (especially BN with its association with impulsivity)

The 'Theme of Anxiety' Trick

When evaluating a patient with anxiety related to eating or food, ask what they are specifically worried about ^[2]:

Worry about gaining weight → Eating disorder
Worry about having a serious illness → Hypochondriasis / illness anxiety disorder
Fear of being poisoned or killed → Paranoid psychosis
Ruminatory guilt or worthlessness → Depression
Associated with intrusive, ego-dystonic obsessional thoughts → OCD
Fear of eating in public / being observed → Social anxiety disorder

The theme directs the diagnosis. This approach is straight from the senior notes ^[2].

This is commonly tested — can you tell AN from BN from BED from ARFID?

Feature	AN Restricting	AN Binge-Purge	BN	BED	ARFID
Body weight	Significantly low	Significantly low	Normal / near-normal	Often overweight/obese	Variable (can be low)
Fear of fatness / body image distortion	✓✓✓	✓✓✓	✓✓	Mild or absent	Absent
Food restriction	Prominent	Present between binges	Present between binges	Not prominent	Present (but for different reasons)
Binge eating	Absent	Present	Present	Present	Absent
Compensatory behaviours	Absent (exercise may be present)	Present	Present	Absent	Absent
Motivation for restriction	Fear of fatness, body control	Fear of fatness, body control	Fear of fatness, body control	N/A	Sensory aversion, fear of choking, lack of interest
Insight	Poor (ego-syntonic)	Poor	Better (ego-dystonic)	Variable	Variable

The weight criterion is the single most important differentiator between AN and BN: if the patient is significantly underweight with binge-purge behaviour, it is AN binge-eating/purging subtype, NOT BN. BN by definition cannot be diagnosed during episodes of AN ^[2].

When a patient presents with weight loss and possible eating disorder, the following investigations help exclude medical mimics ^[2]:

Investigation	What It Excludes
FBC, ESR/CRP	Chronic infection, IBD, malignancy, coeliac disease
TFTs	Hyperthyroidism (↑ T4/T3, ↓ TSH) vs sick euthyroid of AN (↓ T3, normal TSH)
Glucose	Diabetes mellitus (hyperglycaemia), Addison's (hypoglycaemia)
UEC, Ca²⁺, Mg²⁺, PO₄³⁻	Addison's (↑ K⁺, ↓ Na⁺), renal disease, electrolyte consequences of purging
LFTs	Hepatic disease, starvation-related transaminitis
Coeliac screen (anti-tTG, anti-EMA)	Coeliac disease
Cortisol (morning or short Synacthen test)	Addison's disease (↓ cortisol) vs AN (↑ cortisol)
LH, FSH, oestradiol/testosterone	Pituitary failure (low gonadotropins + low sex steroids = hypogonadotropic hypogonadism — but this also occurs in AN from hypothalamic suppression)
MRI Brain	Hypothalamic/pituitary tumours — indicated if atypical presentation (male, very young, no body image distortion, neurological symptoms)
Faecal calprotectin / colonoscopy	IBD (if GI symptoms prominent)

When to Suspect a Medical Mimic Rather Than AN

Consider an organic cause more strongly when:

Male patient (AN is 10:1 F:M — male presentations need careful exclusion of organics)
No over-evaluation of weight/shape (the core psychopathology is absent)
Patient is distressed by weight loss rather than gratified
Unusual age of onset (very young child or adult > 40)
Focal neurological signs, visual field defects, headache
Prominent GI symptoms (bloody diarrhoea, steatorrhoea, severe abdominal pain)
Hyperkalaemia (suggests Addison's — AN/purging typically causes hypoK⁺)
Tachycardia (AN causes bradycardia; tachycardia suggests hyperthyroidism, infection, or other medical cause)

Core psychopathology test: The presence or absence of over-evaluation of weight/shape is the single most important diagnostic discriminator between eating disorders and their mimics.
Weight criterion: Separates AN (significantly underweight) from BN (normal weight) and BED (often overweight).
Compensatory behaviours: Present in AN binge-purge subtype and BN; absent in BED and ARFID.
Motivation for restriction: Fear of fatness (AN/BN) vs sensory aversion/fear of aversive consequences (ARFID) vs loss of appetite from depression/medical illness.
Direction of distress: AN patients are relieved by weight loss; patients with medical conditions or depression are distressed by weight loss.
Physical exam clues: Bradycardia + cold intolerance + lanugo = starvation (AN); tachycardia + heat intolerance + tremor = hyperthyroidism; hyperpigmentation + hyperkalaemia = Addison's; bloody diarrhoea + raised CRP = IBD.

High Yield Summary — Differential Diagnosis

The core psychopathology test (over-evaluation of weight and shape) is the single most important differentiator between eating disorders and their mimics.
Medical mimics of AN: Neoplasia (GI, hypothalamic, lymphoma), IBD, coeliac disease, hyperthyroidism, DM (including "diabulimia"), pituitary failure, chronic infection, Addison's disease, cystic fibrosis.
Psychiatric mimics: Depression (weight loss from anhedonia, no body image distortion), OCD (ego-dystonic obsessions not focused on weight/shape), social anxiety (fear of eating in public, not fear of fatness), BDD (preoccupation with specific body part, not overall weight/shape), psychosis (food refusal from delusions/hallucinations), substance use.
AN vs BN: Weight is the key — AN = significantly low weight; BN = normal weight. BN cannot be diagnosed during episodes of AN.
AN vs ARFID: Both have low weight and restriction. AN = fear of fatness + body image distortion. ARFID = sensory aversion, fear of choking, lack of interest, with NO body image concerns.
Red flags for medical mimic: Male patient, no body image distortion, patient distressed by weight loss, tachycardia, hyperkalaemia, focal neurological signs, atypical age.

Active Recall - Differential Diagnosis of Eating Disorders

References

^[2] Senior notes: ryanho-psych.md (Sections 9.1, 9.1.1 — Eating Disorders, Differential Diagnosis) ^[3] Senior notes: ryanho-psych.md (Section on Body Dysmorphic Disorder) ^[4] Lecture slides: GC 170. Schizophrenia and related psychoses.pdf

Diagnostic Criteria, Algorithm, and Investigations for Eating Disorders

1. Diagnostic Criteria

The diagnosis of eating disorders is clinical — there is no blood test, imaging study, or biomarker that confirms the diagnosis. Instead, we use structured criteria from the DSM-5 (primary) and ICD-10/ICD-11 (supplementary) to ensure systematic, reproducible diagnosis. Investigations serve two purposes: (1) excluding medical differentials and (2) assessing medical complications/severity.

1.1 Anorexia Nervosa — Diagnostic Criteria

Criterion	Description	Why This Criterion Exists
A. Restriction of energy intake	Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Defined as a weight less than minimally normal (adults) or less than minimally expected (children/adolescents)	This captures the behavioural consequence of the core psychopathology — the patient acts on their fear of fatness by restricting. "Significantly low" replaces the old rigid BMI cut-off, allowing clinical judgment
B. Fear of weight gain	Intense fear of gaining weight or of becoming fat, or persistent behaviour that interferes with weight gain, even though at a significantly low weight	This is the motivational engine. Note the DSM-5 addition of "persistent behaviour that interferes with weight gain" — this captures patients who deny fear of fatness (as seen in some Hong Kong/Asian non-fat-phobic AN patients) but whose behaviour clearly demonstrates resistance to weight restoration
C. Body image disturbance	Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of current low body weight	This is the cognitive distortion component — the patient either perceives themselves as fat (perceptual distortion), bases their entire self-worth on weight/shape (cognitive distortion), or simply does not recognise the danger (anosognosia)

Subtypes (specify based on past 3 months) ^[2]:

Restricting type: No recurrent binge-eating or purging. Weight loss accomplished primarily through dieting, fasting, and/or excessive exercise
Binge-eating/Purging type: Recurrent episodes of binge eating or purging behaviour (self-induced vomiting, laxative/diuretic/enema misuse)

Severity specifiers (based on BMI for adults; adapted for children using BMI percentiles) ^[2]:

Severity	BMI
Mild	≥ 17 kg/m²
Moderate	16–16.99 kg/m²
Severe	15–15.99 kg/m²
Extreme	< 15 kg/m²

Remission specifiers ^[2]:

Partial remission: After full criteria previously met, criterion A (low body weight) has not been met for a sustained period but either criterion B or C is still met
Full remission: None of the criteria have been met for a sustained period

For a definite diagnosis, all of the following are required:

Criterion	Description
(a) Low body weight	Body weight maintained ≥ 15% below expected, or BMI ≤ 17.5. Pre-pubertal patients may show failure to make expected weight gain during period of growth
(b) Self-induced weight loss	By avoidance of "fattening food." ≥ 1 of: self-induced vomiting, self-induced purging, excessive exercise, use of appetite suppressants and/or diuretics
(c) Body image distortion	Specific psychopathology whereby a dread of fatness persists as an intrusive, overvalued idea and the patient imposes a low weight threshold on himself/herself
(d) Endocrine disorder	Widespread endocrine disorder involving the HPG axis: amenorrhoea in women, loss of sexual interest and potency in men. Also ↑ GH, ↑ cortisol, changes in thyroid metabolism, abnormalities in insulin secretion
(e) Pubertal delay	If onset is pre-pubertal, the sequence of pubertal events is delayed or arrested. With recovery, puberty is often completed normally but menarche is late

DSM-5 vs ICD-10: Key Differences for AN

Three important changes from ICD-10 to DSM-5 ^[2]:

Amenorrhoea removed from DSM-5 criteria — because (a) it excludes male patients, pre-menarchal girls, and post-menopausal women, (b) some patients develop amenorrhoea only late, and (c) patients on oral contraceptives may continue to have withdrawal bleeds. It still occurs and is clinically important, but is no longer required for diagnosis.
DSM-5 added "persistent behaviour that interferes with weight gain" as an alternative to criterion B — this captures non-fat-phobic AN (relevant to HK/Asian populations who restrict for somatic reasons rather than fat-phobia).
DSM-5 uses flexible "significantly low weight" rather than the rigid "15% below expected" / "BMI ≤ 17.5" threshold — allowing clinical judgment for context (e.g., a previously obese patient who has lost 30% of body weight but still has BMI > 17.5 may qualify).

1.2 Bulimia Nervosa — Diagnostic Criteria

Criterion	Description	Why This Criterion Exists
A. Recurrent binge eating	Characterised by both: (1) Eating, in a discrete period of time (e.g., ≤ any 2-hour period), an amount of food that is definitely larger than what most individuals would eat in a similar period under similar circumstances; (2) A sense of lack of control over eating during the episode	The binge must be both objectively large AND subjectively uncontrolled. This excludes "subjective binges" where the patient feels out of control but the amount is not objectively excessive (those fall under OSFED)
B. Compensatory behaviours	Recurrent inappropriate compensatory behaviours to prevent weight gain: self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise	Without compensation, this would be BED. The compensation is what drives the vicious cycle of BN and causes most of its medical complications
C. Duration/frequency	Binge eating and compensatory behaviours both occur, on average, ≥ 1/week for 3 months	This threshold prevents over-diagnosis of isolated episodes. DSM-IV required 2/week — DSM-5 lowered this to capture more cases
D. Self-evaluation	Self-evaluation is unduly influenced by body shape and weight	The shared core psychopathology with AN — this is what distinguishes BN from other causes of binge eating
E. Not during AN	The disturbance does not occur exclusively during episodes of anorexia nervosa	If the patient meets criteria for AN (significantly low weight), they are diagnosed with AN binge-eating/purging subtype, NOT BN. AN "trumps" BN diagnostically

Severity specifiers (based on frequency of compensatory behaviours per week) ^[2]:

Severity	Compensatory behaviours/week
Mild	1–3
Moderate	4–7
Severe	8–13
Extreme	≥ 14

Remission specifiers ^[2]:

Partial remission: After full criteria previously met, some but not all criteria met for a sustained period
Full remission: None of the criteria met for a sustained period

For a definite diagnosis, all of the following are required:

Criterion	Description
(a) Binge eating	Persistent preoccupation with eating and irresistible craving for food; patient succumbs to episodes of overeating in which large amounts of food are consumed in short periods of time
(b) Compensatory behaviour	Patient attempts to counteract the "fattening" effects of food by ≥ 1 of: self-induced vomiting, purgative abuse, alternating periods of starvation, use of drugs (appetite suppressants, thyroxine, diuretics). In DM patients, may choose to neglect insulin treatment
(c) Psychopathology	Morbid dread of fatness with a sharply defined weight threshold, well below the premorbid weight that constitutes the optimum/healthy weight. There is often but not always a history of earlier AN (interval ranging from months to years) — may have been fully expressed or cryptic with moderate weight loss and/or transient amenorrhoea

ICD-10 Recognises 'Diabulimia'

Note that ICD-10 criterion (b) specifically mentions that diabetic patients may neglect their insulin medications as a form of compensatory behaviour. This is sometimes called "diabulimia" — deliberate insulin omission to induce glycosuria and weight loss. This carries extremely high mortality and must be actively screened for in T1DM patients with unexplained weight loss, recurrent DKA, or poor glycaemic control ^[2].

Criterion	Description
A. Recurrent binge eating	Same definition as BN criterion A: (1) objectively large amount in a discrete period; (2) sense of loss of control
B. Associated features	Binge episodes associated with ≥ 3 of: (1) eating much more rapidly than normal; (2) eating until uncomfortably full; (3) eating large amounts when not physically hungry; (4) eating alone due to embarrassment; (5) feeling disgusted, depressed, or very guilty afterward
C. Marked distress	Marked distress regarding binge eating is present
D. Duration/frequency	Occurs, on average, ≥ 1/week for 3 months
E. No compensation	The binge eating is NOT associated with recurrent inappropriate compensatory behaviours (unlike BN) and does not occur exclusively during AN or BN

Severity specifiers (based on binge episodes/week):

Severity	Binge episodes/week
Mild	1–3
Moderate	4–7
Severe	8–13
Extreme	≥ 14

Key conceptual point: BED is distinguished from BN by the absence of compensatory behaviours. Think of it this way: in BN, the patient binges AND compensates (creating the vicious cycle); in BED, the patient binges but does NOT compensate → weight tends to increase → strong association with obesity.

Criterion	Description
A. Eating/feeding disturbance	Apparent lack of interest in eating or food; avoidance based on sensory characteristics of food; concern about aversive consequences of eating — leading to persistent failure to meet nutritional/energy needs, as manifested by ≥ 1 of: significant weight loss, significant nutritional deficiency, dependence on enteral feeding/oral supplements, marked interference with psychosocial functioning
B. Not explained by	Not better explained by lack of available food or culturally sanctioned practice
C. Not during AN/BN	Does not occur exclusively during AN or BN, and there is no evidence of disturbance in the way body weight or shape is experienced
D. Not due to medical/psychiatric condition	Not attributable to a concurrent medical condition or better explained by another mental disorder

OSFED captures clinically significant eating disorder presentations that do not meet full criteria for AN, BN, or BED:

Category	Description
Atypical anorexia nervosa	All criteria for AN met EXCEPT weight remains within or above the normal range despite significant weight loss
Subthreshold BN	Binge eating and compensatory behaviours occur < 1/week or for < 3 months
Subthreshold BED	Binge eating occurs < 1/week or for < 3 months
Purging disorder	Recurrent purging to influence weight/shape in the absence of binge eating
Night eating syndrome	Recurrent episodes of night eating (eating after awakening from sleep or excessive food consumption after evening meal), causing distress, not explained by external influences or another disorder

Atypical AN — Don't Be Fooled by 'Normal' BMI

Atypical AN is extremely important and commonly missed. A patient who has dropped from BMI 32 to BMI 22 — technically "normal" — may have lost a massive amount of weight through pathological restriction, has all the cognitive features of AN, and may develop the same dangerous medical complications (electrolyte disturbance, bradycardia, QT prolongation). The DSM-5 move away from rigid BMI cut-offs was partly to address this. Always assess the trajectory and percentage of weight lost, not just the absolute number.

The following algorithm outlines the systematic approach to diagnosing eating disorders, from initial presentation through to subtype classification.

Note the hierarchical logic: AN "trumps" BN — if the patient is significantly underweight AND binge-purging, they have AN binge-eating/purging subtype, NOT BN. This is because the starvation state in AN fundamentally changes the medical risk profile and treatment approach ^[2].

Before discussing investigations, remember that the assessment of eating disorders involves three parallel tracks ^[2]:

Track	Purpose	Key Components
1. Eating History	Establish the diagnosis	Eating pattern, restriction, binging, purging, exercise habits, food rituals, weight history ^[2]
2. Psychological Assessment	Assess core psychopathology and comorbidities	Attitude to weight/shape, body image disturbance, motivation, insight, formulation (3P model: predisposing, precipitating, perpetuating factors), mood, anxiety, suicidality, self-harm ^[2]
3. Risk Assessment	Determine severity, setting of care, and urgency	Medical risk (vitals, BMI, ECG, electrolytes), suicide risk, current BMI category, physical examination ^[2]

This framework from the senior notes maps BMI to expected clinical consequences and guides the setting of care:

BMI Category	Clinical Significance	Setting
17.5–20 (Underweight)	Irregular or absent menstruation, ovulation failure	Outpatient if stable
15–17.5 (AN range)	Amenorrhoea, loss of substance from all body organs and structures	Outpatient (if > 16 and no physical complications)
13.5–15 (Severe AN)	All organ systems compromised (bone, heart, muscle, brain)	Day-patient (BMI 14–16 without complications)
12–13.5 (Critical AN)	Organs begin to fail (marrow, muscle, heart) — inpatient treatment recommended	Inpatient
< 12 (Life-threatening AN)	Imminent risk of death	Emergency inpatient

Inpatient care is indicated when there is:

Domain	Specific Alert Criteria
General	BMI < 14 kg/m², Temperature < 35.5°C
Cardiovascular	HR < 40 bpm, BP < 80/50 mmHg, postural hypotension > 20 mmHg, postural tachycardia (increase > 20 bpm), arrhythmia, QTc > 450 msec
Biochemical	K⁺ < 2.5 mmol/L, glucose < 2.5 mmol/L ("hypoGly < 4" for concern level), phosphate < 0.5, Na⁺ < 130, Mg²⁺ < 0.5, neutropenia
Psychiatric	Active suicidal ideation, severe self-harm, inability to cooperate with outpatient treatment

4. Investigations

Investigations in eating disorders serve three purposes:

Exclude medical differentials (is this AN or hypothalamic tumour?)
Assess severity of medical complications (how much damage has starvation/purging caused?)
Monitor during treatment (refeeding syndrome surveillance, response to treatment)

Investigation	Expected Findings in AN	Expected Findings in BN	Pathophysiological Explanation	Alert Values ^[2]
FBC	Normocytic normochromic anaemia, mild leucopenia with relative lymphocytosis, thrombocytopenia ^[2]	Usually normal unless severe purging	Starvation → gelatinous bone marrow transformation → ↓ haematopoiesis across all lineages. Lymphocytes are relatively preserved because they are long-lived cells that depend less on marrow output	Neutropenia (absolute count)
Potassium (K⁺)	May be low if purging subtype	↓↓ (most dangerous finding)	Vomiting: loss of HCl → metabolic alkalosis → renal K⁺ wasting. Laxatives: direct K⁺ loss in stool. Diuretics: renal K⁺ loss	Concern: < 3.5; Alert: < 3.0 ^[2]
Sodium (Na⁺)	↓ (dilutional from water loading, or dehydration)	↓ (laxative/diuretic misuse)	Excess free water intake (some AN patients water-load before weigh-ins), or renal/GI sodium losses from purging	Concern: < 135; Alert: < 130 ^[2]
Magnesium (Mg²⁺)	↓	↓ (purging)	Poor dietary intake + GI/renal losses from purging. Important because hypoMg²⁺ prevents correction of hypoK⁺ (Mg²⁺ is required for the Na⁺/K⁺-ATPase pump)	Concern: 0.5–0.7; Alert: < 0.5 ^[2]
Phosphate (PO₄³⁻)	↓ (especially during refeeding)	Usually normal	Intracellular phosphate is depleted in chronic starvation but serum levels may appear normal because phosphate shifts extracellularly. During refeeding, insulin surge drives phosphate back intracellularly → precipitous drop → refeeding syndrome	Concern: 0.5–0.8; Alert: < 0.5 ^[2]
Urea	↑ (dehydration) or ↓ (protein malnutrition)	↑ (dehydration from purging)	Dehydration → pre-renal state → ↑ urea. Alternatively, very low protein intake → ↓ urea production	Concern: > 7; Alert: > 10 ^[2]
Glucose	↓↓ (hypoglycaemia)	Usually normal	Chronic caloric restriction → depleted hepatic glycogen stores → inability to maintain euglycaemia, especially during fasting	Concern: < 3.5; Alert: < 2.5 ^[2]
Albumin	↓ in severe/chronic cases	Usually normal	Protein malnutrition → ↓ hepatic albumin synthesis. Note: albumin may be falsely preserved if the patient is dehydrated (haemoconcentration)	Concern: < 35; Alert: < 32 ^[2]
Creatinine Kinase (CK)	↑ (if excessive exercise or severe muscle wasting)	Usually normal	Skeletal muscle breakdown (rhabdomyolysis from excessive exercise, or from muscle catabolism in starvation) → release of CK into blood	Concern: > 170; Alert: > 250 ^[2]

Test	Expected Findings	Explanation	Alert Values ^[2]
Bilirubin	↑ in severe starvation	Starvation-related hepatocellular damage (autophagy) or haemolysis	Concern: > 20; Alert: > 40
ALP	↑	Bone turnover (osteoporosis) or hepatic cholestasis	Concern: > 110; Alert: > 200
AST	↑	Hepatocellular damage from starvation (hepatocyte autophagy) or from refeeding (hepatic steatosis)	Concern: > 40; Alert: > 80
ALT	↑	Same as AST — more liver-specific	Concern: > 45; Alert: > 90
GGT	↑	Hepatocellular damage, or concurrent alcohol use (common in BN)	Concern: > 45; Alert: > 90

Why do transaminases rise in starvation? When the body is starved, hepatocytes undergo autophagy (self-digestion of cellular components for energy). This cellular stress and damage releases AST/ALT into the bloodstream. Paradoxically, transaminases can also rise during refeeding because rapid carbohydrate provision causes hepatic steatosis (fat deposition in the liver).

Test	Expected Findings in AN	Explanation
LH, FSH, Oestradiol / Testosterone	All ↓ (hypogonadotropic hypogonadism) ^[2]	Hypothalamic GnRH suppression from energy deficit → ↓ pituitary gonadotropins → ↓ sex steroids. This is functional and reversible with weight restoration
TFTs	↓ T3 (sometimes ↓ T4), normal TSH — "low T3 syndrome" / sick euthyroid syndrome ^[2]	Peripheral conversion of T4 → T3 is reduced as an adaptive mechanism to conserve energy (↓ metabolic rate). TSH remains normal because this is a peripheral adaptation, not primary thyroid disease. Do NOT treat with thyroxine — this is appropriate physiology
Cortisol	↑; dexamethasone non-suppression ^[2]	Chronic starvation = physiological stress → ↑ HPA axis activation → ↑ CRH → ↑ ACTH → ↑ cortisol. The non-suppression mimics Cushing's syndrome (pseudo-Cushing's) but resolves with refeeding
Growth Hormone	↑ GH, ↓ IGF-1 ^[2]	GH resistance in starvation: GH is elevated but IGF-1 (produced by the liver in response to GH) is low because the malnourished liver cannot respond to GH signalling. In pre-pubertal patients, this results in growth failure
Prolactin	Usually normal	Helps exclude prolactinoma as a cause of amenorrhoea

The 'Starvation Endocrinopathy' — Don't Treat It, Feed It

A common mistake is to see the endocrine abnormalities in AN (↓ sex hormones, ↓ T3, ↑ cortisol, ↑ GH) and start hormone replacement or thyroid medication. All of these are adaptive responses to starvation and will normalise with weight restoration. Giving thyroxine to a starving patient is actively dangerous (↑ metabolic rate → accelerated catabolism). Giving oestrogen does not protect bone — only weight restoration does that.

Finding	Pathophysiology	Clinical Significance ^[2]
Sinus bradycardia	↓ Metabolic demand → ↑ vagal tone; ↓ cardiac muscle mass	Concern: HR < 50; Alert: HR < 40 ^[2]
QT prolongation	Electrolyte disturbance (hypoK⁺, hypoMg²⁺, hypoCa²⁺) → delayed ventricular repolarisation	Alert: QTc > 450 msec → risk of torsades de pointes → VF → sudden cardiac death ^[2]
U waves	HypoK⁺ → delayed repolarisation of the Purkinje fibres → small deflection after the T wave	Marker of hypoK⁺
ST segment depression, T wave flattening/inversion	HypoK⁺ effects on cardiac repolarisation	Non-specific but corroborates electrolyte disturbance
Arrhythmias	Electrolyte imbalance + structural cardiac changes (myocardial fibrosis from starvation)	Any arrhythmia = Alert ^[2]

Why is the ECG so important? Because sudden cardiac death is a leading cause of mortality in AN. The combination of structural cardiac changes (↓ cardiac mass, myocardial fibrosis) + electrolyte disturbances (hypoK⁺, hypoMg²⁺) + QT prolongation creates a perfect substrate for fatal arrhythmias. An ECG should be performed at every clinical encounter in severe AN.

Finding	Pathophysiology	Clinical Significance
Osteopenia (T-score −1.0 to −2.5) or Osteoporosis (T-score ≤ −2.5) ^[2]	Multifactorial: (1) ↓ oestrogen → ↑ osteoclast activity; (2) ↑ cortisol → ↓ osteoblast activity; (3) ↓ IGF-1 → ↓ bone formation; (4) ↓ dietary calcium/vitamin D; (5) ↓ mechanical loading if excessive exercise is not weight-bearing	Osteoporosis in AN can develop within 6–12 months of amenorrhoea. May be partially irreversible. Indicated for any patient with AN for > 6–12 months or with history of fragility fracture

Investigation	What It Excludes
TFTs	Hyperthyroidism (↑ T4/T3, ↓ TSH) — a medical cause of weight loss with anxiety
ESR / CRP	Inflammatory conditions (IBD, chronic infection, malignancy) — AN typically has normal inflammatory markers
Coeliac screen (anti-tTG, anti-EMA)	Coeliac disease — cause of malabsorption and weight loss
Blood glucose / HbA1c	Diabetes mellitus — weight loss from insulin deficiency
Morning cortisol / short Synacthen test	Addison's disease — weight loss, fatigue, hypotension (but with ↑ K⁺ and hyperpigmentation)
MRI Brain	Hypothalamic/pituitary tumours — indicated for atypical presentations

These are essentially the same investigations listed in the differential diagnosis section but are worth repeating here to emphasise: every new diagnosis of AN should have baseline TFTs and ESR/CRP at minimum to exclude common medical mimics ^[2].

Investigation	Expected Findings	Explanation
Serum amylase	↑ (specifically salivary isoamylase)	Chronic parotid stimulation from repeated vomiting → parotid hypertrophy → ↑ salivary amylase release. Can be used as a biomarker of purging activity (if the patient denies vomiting)
Venous blood gas / Serum bicarbonate	Metabolic alkalosis (vomiting) or metabolic acidosis (laxative misuse)	Vomiting → HCl loss → ↑ HCO₃⁻ → alkalosis. Laxatives → HCO₃⁻-rich intestinal secretion loss → acidosis
Urine specific gravity	↑ (concentrated — dehydration) or ↓ (dilute — water loading)	Helps assess hydration status and detect water loading (a behaviour where patients drink large volumes before weigh-ins to appear heavier)
Urine electrolytes / laxative screen	May detect surreptitious laxative or diuretic use	Useful when the clinical picture (e.g., metabolic alkalosis with hypoK⁺) suggests purging but the patient denies it

While formal diagnosis uses DSM-5/ICD criteria, screening questionnaires can aid in early detection:

Tool	Description
SCOFF Questionnaire	5 questions: Sick (do you make yourself sick?), Control (do you worry about loss of control?), One stone (have you lost > 1 stone/6.35 kg in 3 months?), Fat (do you believe you are fat?), Food (does food dominate your life?). ≥ 2 "yes" answers = positive screen
EAT-26 (Eating Attitudes Test)	26-item self-report questionnaire; score ≥ 20 suggests disordered eating
EDE-Q (Eating Disorder Examination Questionnaire)	Gold-standard self-report measure of eating disorder psychopathology

Category	Tests	Key Findings
Haematology	FBC	Pancytopenia (marrow suppression) ^[2]
Biochemistry	UEC, Ca²⁺, Mg²⁺, PO₄³⁻	HypoK⁺, hypoNa⁺, hypoMg²⁺, hypoPO₄ ^[2]
Metabolic	Glucose, albumin, cholesterol, carotene, CK	Hypoglycaemia, hypoalbuminaemia, ↑ cholesterol, ↑ carotene ^[2]
Liver	LFTs (Bili, ALP, AST, ALT, GGT)	Starvation hepatitis ^[2]
Endocrine	TFTs, LH/FSH, oestradiol/testosterone, cortisol, GH/IGF-1	Low T3 syndrome, hypogonadism, ↑ cortisol, ↑ GH / ↓ IGF-1 ^[2]
Cardiac	ECG	Bradycardia, QT prolongation, U waves, arrhythmias ^[2]
Purging markers	Amylase, VBG/HCO₃⁻, urine electrolytes	↑ Salivary amylase, metabolic alkalosis/acidosis
Bone	DEXA scan	Osteopenia/osteoporosis ^[2]
Differential diagnosis	TFTs, ESR/CRP, coeliac screen, glucose/HbA1c	Exclude organic causes ^[2]

High Yield Summary — Diagnosis and Investigations

AN diagnosis (DSM-5): Three criteria — (A) significantly low weight from energy restriction, (B) intense fear of weight gain OR persistent behaviour interfering with weight gain, (C) body image disturbance / undue influence of weight on self-evaluation / lack of recognition of seriousness. Subtypes: restricting vs binge-eating/purging. Severity by BMI (mild ≥ 17, extreme < 15).
BN diagnosis (DSM-5): Five criteria — (A) recurrent binge eating (large amount + loss of control), (B) recurrent compensatory behaviours, (C) ≥ 1/week for ≥ 3 months, (D) self-evaluation unduly influenced by weight/shape, (E) does not occur exclusively during AN. Severity by compensatory behaviour frequency/week.
BED vs BN: Both have binge eating; BED has NO compensatory behaviours.
AN vs ARFID: Both have low weight; AN has body image distortion / fat-phobia; ARFID does not.
DSM-5 removed amenorrhoea from AN criteria (but it still occurs clinically). DSM-5 added "persistent behaviour interfering with weight gain" to capture non-fat-phobic AN.
Key investigations and alert values: K⁺ < 3.0, PO₄ < 0.5, glucose < 2.5, HR < 40, QTc > 450 msec, BMI < 14, temperature < 35.5°C → urgent intervention / inpatient.
Starvation endocrinopathy: ↓ T3, ↓ LH/FSH/sex steroids, ↑ cortisol, ↑ GH / ↓ IGF-1 — all resolve with refeeding. Do NOT treat with hormones.
Vomiting → ↑ salivary amylase + metabolic alkalosis; laxatives → metabolic acidosis.
SCOFF mnemonic for screening: Sick, Control, One stone, Fat, Food.

Active Recall - Diagnostic Criteria, Algorithm, and Investigations

References

Management of Eating Disorders

The management of eating disorders follows four fundamental components, delivered simultaneously and adapted to the severity, setting, and specific diagnosis ^[2]:

Management of medical complications — the acute life-saving priority
Nutritional rehabilitation — restoring weight and normalising eating patterns
Education and psychotherapy — the mainstay of long-term treatment
Medications — as adjunct only, with limited evidence in most contexts

The overarching principle is this: eating disorders are ego-syntonic (especially AN), meaning the patient often does not want treatment. The therapeutic approach must therefore be empathic, non-judgmental, and motivational — you cannot simply tell a patient with AN to eat more, just as you cannot tell a patient with a phobia to stop being afraid. You must work with their ambivalence ^[2].

"The patient is often ambivalent or reluctant — offer an empathic approach" ^[2]. This is not soft psychiatry — it is evidence-based. Confrontational approaches increase dropout rates and worsen outcomes.

The setting of care is determined by BMI and the presence of physical complications — this is a crucial decision because it determines the intensity of monitoring and the feasibility of treatment ^[2].

Setting	Criteria	Rationale
Inpatient	BMI ≤ 14 or physical complications: K⁺ < 2.5, arrhythmia, hypoglycaemia < 4 (alert < 2.5), HR < 40, ↑ QTc ( > 450 msec), active suicidality, failed outpatient treatment	At this level of malnutrition, organ failure is imminent or present. Refeeding must be supervised to prevent refeeding syndrome. Continuous cardiac monitoring is essential. Psychiatric risk (suicide) is also very high in this population ^[2]
Day-patient	BMI 14–16 and no physical complications	Patient is medically stable enough not to require 24-hour monitoring, but still needs meal supervision and multidisciplinary assessment in a structured environment ^[2]
Outpatient	BMI > 16 and no physical complications	The majority of eating disorder patients can be managed as outpatients. This requires adequate motivation (or at least ambivalence that can be worked with), a safe home environment, and access to specialist services ^[2]

When to Admit — The Critical Numbers

Memorise these alert values — they determine immediate life-saving decisions ^[2]:

BMI < 14 kg/m² → inpatient
HR < 40 bpm → inpatient
K⁺ < 2.5 mmol/L → urgent correction
QTc > 450 msec → cardiac monitoring
Glucose < 2.5 mmol/L → emergency
Temperature < 35.5°C → inpatient
Any arrhythmia → cardiac monitoring
Neutropenia → infection risk

4. Component 1: Management of Medical Complications

Medical stabilisation is the first priority — you cannot do psychotherapy with a patient who is about to have a cardiac arrest.

Emergency	Management	Rationale
Severe hypokalaemia (K⁺ < 2.5)	IV potassium chloride (max 40 mmol/hr via central line; 10–20 mmol/hr peripherally), cardiac monitoring	HypoK⁺ → QT prolongation → torsades de pointes → VF → death. Must also correct hypoMg²⁺ simultaneously (Mg²⁺ is needed for Na⁺/K⁺-ATPase function; hypoK⁺ is refractory to correction without Mg²⁺ repletion)
Severe hypoglycaemia (glucose < 2.5)	IV dextrose (50 mL of 50% dextrose), then maintenance dextrose infusion; transition to supervised oral intake	Depleted hepatic glycogen cannot maintain euglycaemia. IV dextrose provides immediate substrate
Cardiac arrhythmia / QT prolongation	Continuous telemetry, correct electrolytes (K⁺, Mg²⁺, Ca²⁺), withhold QT-prolonging medications	The arrhythmia substrate is electrolyte-driven — correct the cause
Severe bradycardia (HR < 40)	Bed rest (to reduce metabolic demand), continuous monitoring, consider atropine if haemodynamically unstable	Starvation bradycardia is usually vagally mediated and benign, but at HR < 40 there is risk of asystole or unstable rhythms
Hypothermia (Temp < 35.5°C)	Active warming (warm blankets, warm IV fluids), treat underlying cause (starvation)	↓ Metabolic rate → ↓ thermogenesis. Hypothermia itself can cause arrhythmias

Daily monitoring in inpatients: weight (after voiding, in hospital gown), vitals (HR, BP including postural, temperature), fluid balance
Regular blood tests: UEC (especially K⁺, Mg²⁺, PO₄³⁻), glucose, LFTs — frequency depends on severity (daily in acute phase, then weekly)
ECG: At baseline and whenever electrolytes change or clinical deterioration occurs
Management of osteoporosis: Weight restoration is the primary treatment (normalises oestrogen, cortisol, IGF-1). Bisphosphonates are generally NOT recommended in young patients (teratogenic; long bone half-life). Calcium and vitamin D supplementation as adjunct. HRT does NOT protect bone in the absence of weight restoration
Dental review: For patients with purging behaviour — fluoride rinse, avoid brushing immediately after vomiting (enamel is softened by acid)

5. Component 2: Nutritional Rehabilitation

This is the cornerstone of physical recovery. The goal is controlled weight restoration while avoiding refeeding syndrome — the most dangerous iatrogenic complication in eating disorder management.

Parameter	Recommendation	Rationale
Starting caloric intake	Start low: 5–10 kcal/kg/day (often ~1000 kcal/day for severe AN with BMI < 14); some guidelines support 1200–1500 kcal/day for less severe cases	Starting too high risks refeeding syndrome. Starting too low risks underfeeding syndrome (continued catabolism). Recent evidence suggests moderate initial caloric intake (1200–1500 kcal/day) may be safe with appropriate monitoring
Rate of increase	Increase by 200–300 kcal every 2–3 days	Gradual upward titration allows metabolic adaptation and monitoring for refeeding complications
Target weight gain	Inpatient: 0.5–1.0 kg/week; outpatient: 0.25–0.5 kg/week	Faster gain risks fluid overload and refeeding syndrome. Slower gain prolongs the medical risk period
Target BMI	BMI 19–20 as initial weight restoration goal (for return of menses, normalisation of endocrine function)	Below this, the HPG axis remains suppressed and medical complications persist
Route	Oral feeding preferred (food, not supplements). Nasogastric (NG) feeding only if oral feeding fails or medical emergency	Oral feeding is both nutritionally and psychologically therapeutic — it directly addresses the behavioural component. NG feeding bypasses the psychological work but is sometimes necessary

Refeeding syndrome is a potentially fatal constellation of metabolic derangements occurring when nutrition is re-introduced to a severely malnourished patient.

Pathophysiology — Why does it happen?

During starvation:

The body switches from carbohydrate to fat/protein metabolism
Intracellular stores of phosphate, potassium, magnesium, and thiamine are depleted
Serum levels may appear normal (because of extracellular shift and reduced renal clearance)

When carbohydrate is re-introduced:

Insulin surges (glucose → insulin release)
Insulin drives glucose, phosphate, potassium, and magnesium intracellularly (for glycolysis, ATP synthesis, and protein synthesis)
Serum levels plummet → hypophosphataemia (most characteristic), hypokalaemia, hypomagnesaemia
Thiamine (vitamin B1) is a cofactor for glucose metabolism; increased glucose metabolism without adequate thiamine → Wernicke's encephalopathy
Insulin also causes renal sodium and water retention → fluid overload → oedema, cardiac failure ^[2]

The mnemonic for refeeding syndrome manifestations: "PHASE" — Phosphate low, Hypokalaemia, Arrhythmias, Sodium/water retention (oedema), Encephalopathy (Wernicke's from thiamine depletion)

Prevention of refeeding syndrome ^[2]:

Measure	Rationale
Thiamine supplementation — give BEFORE refeeding (200–300 mg IV/oral daily for ≥ 5 days)	Thiamine is a cofactor for pyruvate dehydrogenase and transketolase. Carbohydrate loading without thiamine → Wernicke's encephalopathy (confusion, ophthalmoplegia, ataxia)
Phosphate supplementation — prophylactic oral phosphate; IV if serum PO₄ < 0.5	Prevent the precipitous phosphate drop that is the hallmark of refeeding syndrome
Start low, go slow — caloric intake begins at 5–10 kcal/kg/day in high-risk patients	Limits the insulin surge that drives electrolytes intracellularly
Daily monitoring of PO₄, K⁺, Mg²⁺, Na⁺, glucose for at least the first 7–10 days	Catch derangements early before clinical deterioration
Fluid restriction in the first week (avoid IV fluids unless essential)	Refeeding causes sodium/water retention → fluid overload → cardiac failure. Restrict to ~20–30 mL/kg/day initially
Correct electrolytes aggressively before and during refeeding	Pre-existing depletion + refeeding-driven intracellular shift = dangerous drop

Refeeding Syndrome — The Exam Favourite

Refeeding syndrome is one of the highest-yield topics in eating disorder management. The key facts:

Most characteristic finding: Hypophosphataemia (PO₄ plummets when insulin drives phosphate intracellularly after carbohydrate reintroduction)
Most dangerous consequence: Cardiac arrhythmia / cardiac failure (from electrolyte disturbance + fluid overload)
Prevention: Thiamine BEFORE refeeding, start low go slow, daily electrolyte monitoring, prophylactic phosphate supplementation
Risk group: BMI < 14, very low/absent caloric intake for > 5 days, pre-existing electrolyte derangements ^[2]

Intervention	Mechanism / Rationale
Regular weighing	Provides objective feedback; helps both clinician and patient track progress. Usually 1–2x/week (not daily — daily fluctuations cause anxiety) ^[2]
Homework: food diary keeping and problem-solving	Self-monitoring of eating patterns, thoughts, and feelings around food. Identifies triggers for restriction/bingeing/purging. Provides data for CBT sessions ^[2]
Token economy and nurse supervision	Behavioural reinforcement: controlled weight gain rewarded with privileges (e.g., increased activity, visits). Supervised meals and snacks by nursing staff during and after meals (to prevent purging). MDT-supervised approach ^[2]
Supported eating	Repeated exposure to food and the act of eating to overcome anxiety. Based on extinction learning — repeated exposure without the feared consequence (weight gain is reframed) → gradual reduction in food-related anxiety ^[2]
Meal supervision	Extends supported eating to home and school environments by carers, school staff, or trusted friends. Ensures eating occurs and purging is prevented ^[2]

Aim of behavioural interventions: To rebuild normal hunger and satiety signals and control over eating → achieve normal social eating with the right amount and variety of food ^[2].

6. Component 3: Education and Psychotherapy — The Mainstay of Treatment

Education and psychotherapy are the mainstay of treatment for eating disorders ^[2]. Medications have a limited role. The choice of psychotherapy depends on the diagnosis and the patient's age.

6.1 Psychotherapy for Anorexia Nervosa

This is the gold-standard first-line treatment for adolescent AN — it has the strongest evidence base ^[2].

Why family therapy for adolescents?

Adolescents live at home; the family is the primary environment where eating occurs
AN in adolescents is conceptualised as a family problem — not blaming the family, but recognising that the family is the most powerful resource for change
Parents are empowered as the agents of change (rather than the patient, who is ambivalent)

Maudsley Family Therapy — divided into 3 phases ^[2]:

Phase	Focus	Duration	What Happens
Phase I: Weight restoration	Danger of severe malnutrition; assist parents in refeeding the child	Usually ~12 months	The therapist helps the family understand the medical danger. Parents take full control of feeding — they decide what, when, and how much the child eats. The child is temporarily "externalised" from the illness ("the eating disorder is making your daughter refuse food, not your daughter"). Family meals are observed and coached ^[2]
Phase II: Returning control to the adolescent	Starts when patient accepts parental authority over eating and weight is stabilising	Variable	Parents are encouraged to help the child take more control over eating once again — gradually and stepwise. The adolescent begins to make some food choices independently while parents remain involved ^[2]
Phase III: Establishing healthy adolescent identity	Starts when body weight normalises	Variable	Focus shifts from food and weight to broader adolescent developmental issues — identity, autonomy, peer relationships, academic life. Supports increased personal autonomy ^[2]

Outcomes: Adolescent AN with FBT: 60% well at 1 year, 90% well at 5 years ^[2] — the best outcomes of any treatment for any eating disorder.

For adults with AN, individual psychotherapy is superior to specialist or dietary treatment alone → 30% well at 1 year, 40–50% well at 5 years ^[2].

Therapy	Description	Mechanism
CBT-E (Enhanced Cognitive Behavioural Therapy)	The first transdiagnostic eating disorder therapy — can be used for AN, BN, BED, and OSFED ^[2]	Challenges dysfunctional thoughts (e.g., "If I eat this, I will become fat") and addresses dysfunctional behaviours (restriction, purging, body checking). Effective for weight restoration and maintenance. Also effective for BN ^[2]
MANTRA (Maudsley Model of Anorexia Nervosa Treatment for Adults)	Newer treatment specifically for adult AN ^[2]	Focuses on underlying difficulties: interpersonal difficulties, negative self-perception, experience of negative emotions. Uses motivational interviewing, rolling with resistance, empowering the patient. Addresses the maintenance factors of AN (perfectionism, cognitive rigidity, avoidance of emotion) ^[2]
SSCM (Specialist Supportive Clinical Management)	Combines clinical management (weight monitoring, nutritional advice) with supportive therapy	Addresses the patient's concerns in a non-prescriptive way while ensuring medical safety. Sometimes used as a comparison treatment in trials but is effective in its own right
Other psychotherapies	Interpersonal therapy, cognitive analytic therapy, acceptance and commitment therapy, cognitive remediation therapy ^[2]	Interpersonal therapy addresses relationship patterns; cognitive remediation targets cognitive rigidity (a core trait in AN — "set-shifting" difficulty)

Address underlying family issues behind AN ^[2]
Common family dynamics: enmeshment, overprotectiveness, rigidity, lack of conflict resolution
The therapy is NOT about blaming the family — it is about mobilising the family as a resource

Therapy	Description	Evidence
CBT-BN / CBT-E	First-line psychotherapy for BN ^[2]^[5]	Targets the vicious cycle: identifies triggers for bingeing, challenges distorted cognitions about weight/shape, develops alternative coping strategies, normalises eating patterns. Typically 16–20 sessions. Remission rates: ~40–50%
Interpersonal Therapy (IPT)	Focuses on interpersonal problems (grief, role disputes, role transitions, interpersonal deficits) that maintain the disorder ^[5]	Equally effective to CBT at long-term follow-up but slower to take effect. Good alternative for patients who do not respond to or cannot engage with CBT
Guided self-help	Based on CBT principles but delivered through a manual/workbook with limited therapist support	Cost-effective first step; may be sufficient for mild BN

Therapy	Description	Evidence
CBT-BED	Adapted CBT targeting binge eating without the purging cycle	First-line; reduces binge frequency but may not result in significant weight loss
Guided self-help	CBT-based workbook	Recommended as initial step (NICE guidelines)
IPT	Addresses interpersonal triggers for binge eating	Alternative to CBT
Behavioural weight loss programmes	Structured dietary and exercise interventions	Address obesity but may not address underlying psychological drivers; risk of triggering more restrictive eating

Measure	Purpose
Basic psychoeducation	Explain the illness, its consequences, and treatment rationale to patient and family ^[2]
Involvement of multidisciplinary team: nurse, dietician, clinical psychologist, occupational therapist, Red Cross Hospital School teachers, medical social worker	Eating disorders require coordinated multi-professional input. No single discipline can address all aspects ^[2]
Liaison and support in school	BMI goal for returning to school (to ↓ risk of relapse); meal supervision by school staff or trusted friend; physical health monitoring ^[2]
Self-help, support groups, day camps	Peer support, normalisation, shared coping strategies ^[2]
Online support	Accessible, especially for patients with social anxiety ^[2]
Day hospital support	Meal supervision, multidisciplinary assessment for patients between inpatient and outpatient ^[2]
Peer support from recovered patients	Models of recovery; reduces hopelessness ^[2]

7. Component 4: Medications

Medications have a limited role in eating disorders and may be useful as an adjunct for severe cases or those refractory to psychotherapy ^[2]. Psychotherapy is ALWAYS the primary treatment.

Medication	Mechanism	Efficacy	Indications	Contraindications / Cautions
Olanzapine	↑ Appetite via anti-H₁ effect (histamine H₁ receptor blockade in the hypothalamus removes the satiety-promoting effect of histamine → ↑ hunger). Also 5-HT₂A/₂C antagonism → may ↓ anxiety	↑ Weight gain, ↓ AN rumination, ↓ OC symptoms ^[2]	Adjunct in AN when psychotherapy alone is insufficient; particularly when there is severe anxiety, obsessional symptoms, or rumination about food/weight	Metabolic syndrome risk (but less relevant in underweight AN patients); QT prolongation risk (must correct electrolytes first); sedation (may be beneficial for insomnia in AN)
Other antipsychotics (e.g., chlorpromazine)	↑ Appetite (anti-H₁ and anti-D₂ effects)	Little evidence for effect (no significant ↑ weight gain) ^[2]	Rarely used; historical use largely replaced by olanzapine	QT prolongation (chlorpromazine is a potent QT prolonger — dangerous in a population already at risk); postural hypotension; sedation
Antidepressants (e.g., fluoxetine)	SSRI: ↑ synaptic 5-HT by blocking SERT	Little evidence for effect in AN (no significant ↑ weight gain, no ↓ relapse rate) ^[2]	May be considered for comorbid depression or OCD AFTER weight restoration (SSRIs are ineffective in the malnourished state because tryptophan — the 5-HT precursor — is depleted in starvation; there is insufficient substrate for the drug to work on)	Avoid in acute starvation — ineffective due to ↓ tryptophan. Risk of QT prolongation (citalopram, escitalopram — avoid in hypoK⁺). Risk of hyponatraemia (SIADH)

Why Don't SSRIs Work in Starving AN Patients?

SSRIs work by blocking the serotonin transporter (SERT), thereby increasing synaptic serotonin. But serotonin is synthesised from tryptophan (an essential amino acid obtained from dietary protein). In a starving patient, tryptophan levels are severely depleted → there is insufficient serotonin being produced for the SSRI to "keep" in the synapse. This is why SSRIs are ineffective during acute AN but may have a role AFTER weight restoration, when tryptophan levels normalise and serotonin synthesis resumes ^[2].

Medication	Mechanism	Efficacy	Indications
Fluoxetine 60 mg/day	SSRI: ↑ synaptic 5-HT → ↓ binge-purge urges, ↓ impulsivity, ↑ satiety signalling, treats comorbid depression	First-line pharmacotherapy for BN (NICE-recommended). Reduces binge/purge frequency by ~50%. The dose required (60 mg) is higher than for depression (20 mg) — likely because the serotonergic deficit in BN is greater	As adjunct to CBT-BN, or as monotherapy when psychotherapy is unavailable, refused, or ineffective
Other SSRIs (sertraline, citalopram)	Same mechanism as fluoxetine	Moderate evidence; less studied than fluoxetine specifically for BN	Alternative if fluoxetine is not tolerated
Topiramate	Anticonvulsant; mechanism in BN unclear — possibly ↓ appetite via glutamate/GABA modulation, ↑ satiety	Reduces binge/purge frequency; causes weight loss (an advantage over some alternatives but a risk in underweight patients)	Second-line; useful if weight is a concern. Contraindicated in patients with kidney stones

Fluoxetine for BN — 60 mg, Not 20 mg

A common mistake is to prescribe fluoxetine at the standard antidepressant dose (20 mg) for BN. The evidence-based dose for BN is 60 mg/day — this is the dose shown to reduce binge-purge frequency in clinical trials. The higher dose is required because the 5-HT dysfunction in BN is more pronounced than in uncomplicated depression.

Medication	Mechanism	Efficacy	Notes
Lisdexamfetamine (Vyvanse)	Prodrug of dexamphetamine (a CNS stimulant); ↑ DA and NE → ↓ appetite, ↑ executive control/impulse inhibition	Only FDA-approved medication for BED (2015). Reduces binge days/week. Dose: 50–70 mg/day	Not indicated for weight loss per se. Contraindicated in cardiovascular disease, uncontrolled hypertension, hyperthyroidism, glaucoma, history of stimulant abuse. Schedule II controlled substance — abuse potential
SSRIs (fluoxetine, sertraline)	↑ Synaptic 5-HT → ↓ binge eating urges	Moderate evidence; reduces binge frequency	Off-label for BED; may be first-line where lisdexamfetamine is unavailable
Topiramate	Anticonvulsant; ↓ appetite	Reduces binge frequency and weight	Off-label; cognitive side effects ("topira-mate makes you top-dum" — word-finding difficulty, cognitive slowing)

Drug	Key Cautions in Eating Disorder Patients	Why
Any QT-prolonging drug (citalopram, escitalopram, chlorpromazine, haloperidol, methadone)	Extremely dangerous in patients with hypoK⁺, hypoMg²⁺	These patients already have QT prolongation from electrolyte disturbance → adding QT-prolonging drugs dramatically increases the risk of torsades de pointes
SSRIs in acute AN	Ineffective; potentially harmful	↓ Tryptophan → no substrate for SSRI to work; risk of hyponatraemia (SIADH); risk of QT prolongation
Bupropion	Contraindicated in BN and AN	Bupropion lowers the seizure threshold; purging-related electrolyte disturbances (especially hypoNa⁺) also lower seizure threshold → dramatically increased seizure risk. This is explicitly contraindicated
TCAs	Generally avoided	Cardiotoxic (Na⁺ channel blockade); dangerous in patients with QT prolongation and electrolyte disturbance
Stimulants (lisdexamfetamine, methylphenidate)	Abuse potential; appetite suppression	Must be carefully assessed in patients with comorbid substance use or AN features; appetite suppression could worsen restrictive eating

Bupropion is CONTRAINDICATED in Bulimia

This is a classic exam question. Bupropion (Wellbutrin) is contraindicated in BN (and AN) because it lowers the seizure threshold. Purging behaviour causes electrolyte disturbances (hypoNa⁺, hypoK⁺) that also lower the seizure threshold. The combination dramatically increases seizure risk. This is one of the few absolute contraindications in psychiatric prescribing.

8. Disorder-Specific Management Summary

Component	Adolescent	Adult
First-line psychotherapy	Maudsley Family Therapy (FBT) — 3 phases ^[2]	CBT-E or MANTRA ^[2]
Alternative psychotherapy	Individual therapy if family therapy refused/fails	Interpersonal therapy, cognitive analytic therapy, SSCM ^[2]
Nutritional rehabilitation	Supervised refeeding; target 0.5–1 kg/week inpatient	Same
Medications	Olanzapine as adjunct (↑ appetite, ↓ rumination) ^[2]; antidepressants have little evidence	Same
Outcomes	60% well at 1 year, 90% well at 5 years with FBT ^[2]	30% well at 1 year, 40–50% well at 5 years ^[2]

Component	Recommendation
First-line	CBT-BN or CBT-E (16–20 sessions) ^[2]
Alternative psychotherapy	IPT (equally effective long-term, slower onset)
First-line medication	Fluoxetine 60 mg/day — as adjunct to CBT or as monotherapy if psychotherapy unavailable
Guided self-help	CBT-based; appropriate for mild cases as initial step
Key medications to AVOID	Bupropion (seizure risk); QT-prolonging drugs if hypoK⁺

Component	Recommendation
First-line	Guided self-help (CBT-based) or CBT-BED
Medication	Lisdexamfetamine (only FDA-approved drug for BED); SSRIs (fluoxetine, sertraline) as alternatives
Combined approach	CBT + medication may be more effective than either alone
Weight management	Address obesity with structured programmes, but avoid overly restrictive dieting (may trigger binge episodes)

Parameter	Frequency	Purpose
Weight	1–2x/week (inpatient); weekly to fortnightly (outpatient)	Track weight restoration; detect refeeding oedema
Electrolytes (K⁺, Na⁺, Mg²⁺, PO₄)	Daily (first 7–10 days of refeeding); then weekly → monthly	Detect refeeding syndrome; monitor purging complications
ECG	At baseline; repeat with any electrolyte change or clinical concern	QT monitoring; arrhythmia detection
LFTs	Weekly during refeeding; then monthly	Starvation hepatitis → refeeding hepatitis (transaminase flare during refeeding due to hepatic steatosis)
DEXA scan	At diagnosis if AN > 6–12 months; repeat every 1–2 years	Track bone density; guide duration of treatment
Menstrual status	At each visit	Return of menses is a biomarker of adequate weight restoration and HPG axis recovery
Psychological assessments	Regular (with psychotherapy sessions)	Track eating disorder psychopathology, depression, anxiety, quality of life

10. Special Considerations

AN patients may lack insight and refuse treatment even when critically ill
In Hong Kong, involuntary admission can be considered under the Mental Health Ordinance if the patient has a mental disorder (AN qualifies) and is at risk to self (starvation = risk of death)
This is a last resort — ethical tension between autonomy and beneficence. In practice, most patients can be engaged through motivational interviewing and empathic engagement

AN patients with amenorrhoea are assumed to be infertile — but ovulation can occur unpredictably even before menses resume
AN/BN in pregnancy: ↑ risk of miscarriage, IUGR, preterm delivery, low birth weight, perinatal mortality, postnatal depression
Management: specialist obstetric-psychiatric joint care; nutritional rehabilitation; avoid medications with teratogenic risk

~20% of AN patients develop a chronic, treatment-refractory course
Management shifts towards harm reduction and quality of life optimisation rather than cure
Palliative approaches may be appropriate for end-stage AN with repeated failed treatments — ethically complex

High Yield Summary — Management

Setting of care: Inpatient if BMI ≤ 14 or physical complications (K⁺ < 2.5, HR < 40, arrhythmia, QTc > 450, glucose < 2.5). Day-patient if BMI 14–16 without complications. Outpatient if BMI > 16 without complications.
Four components: Medical complication management, nutritional rehabilitation, psychotherapy (mainstay), medications (adjunct only).
Refeeding syndrome: Caused by insulin surge driving phosphate/K⁺/Mg²⁺ intracellularly after carbohydrate reintroduction in starved patients. Most characteristic finding = hypophosphataemia. Prevention: thiamine BEFORE refeeding, start low go slow, daily electrolyte monitoring.
Adolescent AN: First-line = Maudsley Family Therapy (3 phases: weight restoration → returning control → healthy identity). Outcomes: 60% well at 1 year, 90% at 5 years.
Adult AN: First-line = CBT-E or MANTRA. Outcomes: 30% well at 1 year, 40–50% at 5 years.
BN: First-line = CBT-BN/CBT-E. First-line medication = fluoxetine 60 mg/day (NOT 20 mg).
BED: First-line = guided self-help / CBT-BED. FDA-approved medication = lisdexamfetamine.
Olanzapine is the most evidence-supported medication for AN (↑ appetite via anti-H₁, ↓ rumination, ↓ OC symptoms). Antidepressants have little evidence in acute AN.
Bupropion is CONTRAINDICATED in BN and AN (↓ seizure threshold + electrolyte disturbance = seizure risk).
SSRIs are ineffective in starving AN patients (↓ tryptophan → no substrate for SSRI to act on). Only consider after weight restoration.

Active Recall - Management of Eating Disorders

References

^[2] Senior notes: ryanho-psych.md (Sections 9.1, 9.1.1, 9.1.2 — Eating Disorders: Approach to Management, Nutritional rehabilitation, Psychotherapy, Medications, Maudsley Family Therapy, CBT-E, MANTRA, Bulimia Nervosa management) ^[5] Senior notes: ryanho-psych.md (Section 3.3.4 — Indications for Psychotherapy; Section 3.1.1 — Antidepressants)

Complications of Eating Disorders

Complications of eating disorders arise from three mechanistic sources, and understanding which source drives which complication is the key to systematising this topic:

Starvation — the direct effects of chronic caloric deficit on every organ system (predominantly AN)
Purging behaviours — the damage caused by repeated vomiting, laxative abuse, or diuretic misuse (predominantly BN and AN binge-purge subtype)
Iatrogenic / treatment-related — primarily refeeding syndrome, the most dangerous complication of treatment itself

Additionally, there are psychiatric complications (comorbidities that worsen or develop as a consequence of the eating disorder) and long-term sequelae that may persist even after recovery.

Before discussing organ-specific complications, the most important fact: anorexia nervosa carries the highest mortality of ALL psychiatric disorders ^[2].

Parameter	AN	BN
Standardised Mortality Ratio	23.14× general population ^[2]	2–8× general population ^[2]
Average age at death	34 years ^[2]	Variable
Major causes of death	Suicide (32%), anorexia/starvation (19%), cancer (11%) ^[2]	Suicide (~1%), electrolyte-related cardiac death
Suicide	22% lifetime risk of DSH; suicide is the leading cause of death ^[2]	Lower than AN but still elevated

Why is suicide the leading cause of death in AN, not starvation itself? Because AN is associated with profound comorbid depression, anxiety, hopelessness, social isolation, and treatment resistance. By the time patients reach critical BMI, many have endured years of suffering. The chronic neurobiological effects of starvation (5-HT dysfunction, hypercortisolaemia) also directly contribute to depression and suicidality.

These complications arise from chronic caloric deficit. The body systematically shuts down non-essential functions and cannibalises its own tissues for energy. Understanding the order in which organ systems fail at different BMI thresholds is clinically important for risk stratification ^[2]:

BMI	Organ Systems Affected	Clinical Significance ^[2]
17.5–20 (Underweight)	HPG axis: irregular/absent menstruation, ovulation failure	Fertility impaired; bone loss begins
15–17.5 (AN range)	All organs: loss of substance from all body organs and structures; amenorrhoea established	Significant medical risk; outpatient management may still be possible
13.5–15 (Severe AN)	All organ systems compromised: bone, heart, muscle, brain	High medical risk; consider day-patient or inpatient
12–13.5 (Critical AN)	Organs begin to fail: marrow (cytopenias), muscle (cardiac/skeletal), heart (arrhythmia)	Inpatient treatment recommended ^[2]
< 12 (Life-threatening AN)	Imminent multi-organ failure	Emergency inpatient; risk of death ^[2]

Complication	Pathophysiology	Clinical Consequence
Bradycardia	↓ Metabolic demand → compensatory ↑ vagal tone + ↓ cardiac muscle mass → ↓ heart rate	Usually asymptomatic until HR < 40 bpm → risk of haemodynamic instability, syncope, cardiac arrest. Alert: HR < 40 ^[2]
Hypotension and postural hypotension	↓ Intravascular volume (dehydration) + ↓ cardiac output + impaired autonomic vasoconstrictor reflex (autonomic neuropathy from starvation)	Dizziness, syncope, falls. Alert: BP < 80/50, postural drop > 20 mmHg ^[2]
QT prolongation	Electrolyte disturbances — hypoK⁺, hypoMg²⁺, hypoCa²⁺ — delay ventricular repolarisation (phase 3 of the cardiac action potential requires K⁺ efflux; low extracellular K⁺ → slower efflux → prolonged repolarisation)	QTc > 450 msec → risk of torsades de pointes → ventricular fibrillation → sudden cardiac death ^[2]. This is the mechanism of sudden death in AN
Cardiac arrhythmias	Combined structural (myocardial fibrosis, ↓ cardiac mass) and functional (electrolyte-driven) substrate for re-entrant circuits and triggered activity	Any arrhythmia = alert ^[2]. Includes SVT, VT, VF, AF
Mitral valve prolapse	↓ Left ventricular mass → the mitral valve leaflets become relatively too large for the shrunken ventricle → prolapse	Mid-systolic click, late systolic murmur. Usually benign and reversible with weight restoration
Pericardial effusion	Starvation-related serous fluid accumulation; mechanism unclear but related to hypoalbuminaemia and altered capillary permeability	Usually small and asymptomatic; rarely causes tamponade
Heart failure during refeeding	Rapid fluid/calorie reintroduction → insulin-mediated Na⁺/water retention → volume overload on a heart with reduced muscle mass and compliance → congestive cardiac failure	A refeeding complication (see section 4)

Why Does AN Cause Sudden Cardiac Death?

The lethal pathway is: starvation → electrolyte depletion (K⁺, Mg²⁺) → QT prolongation → torsades de pointes → ventricular fibrillation → cardiac arrest. This can happen at any time, even during sleep. It is why ECG and electrolyte monitoring are mandatory in severe AN, and why any QT-prolonging medication is extremely dangerous in this population ^[2].

Complication	Pathophysiology	Reversibility
Amenorrhoea (F) / ↓ libido and impotence (M)	Chronic energy deficit → ↓ leptin → suppression of hypothalamic GnRH pulsatility → ↓ LH/FSH → hypogonadotropic hypogonadism → ↓ oestrogen (F) / ↓ testosterone (M) ^[2]	Reversible with weight restoration. Menses typically return at BMI ~19–20, though may take 6–12 months after weight restoration
Infertility	Anovulation secondary to HPG axis suppression	Reversible in most cases; fertility normalises after weight restoration, though may take time
↑ Cortisol and dexamethasone non-suppression	Starvation = chronic stress → ↑ CRH → ↑ ACTH → ↑ cortisol; also ↓ cortisol clearance	Reversible with weight restoration. Pseudo-Cushing's — must not be confused with true Cushing's syndrome
Hypoglycaemia	↓ Hepatic glycogen stores from chronic caloric restriction → inability to maintain euglycaemia during fasting ^[2]	Immediate danger — can cause seizures, coma, death. Alert: glucose < 2.5 ^[2]
Low T3 syndrome (sick euthyroid)	↓ Peripheral conversion of T4 → T3 (adaptive mechanism to conserve energy by ↓ metabolic rate). TSH remains normal ^[2]	Reversible with weight restoration. Do NOT treat with thyroxine
↑ GH, ↓ IGF-1	GH resistance: GH is elevated but the malnourished liver cannot produce IGF-1 in response. In children → growth failure and short stature ^[2]	Growth may be permanently impaired if AN occurs during critical growth window (pre-pubertal/pubertal)
Stunted growth and failure of breast development	If onset is pre-pubertal: combined effect of ↓ IGF-1 (growth) + ↓ oestrogen (puberty) → pubertal delay or arrest ^[2]	Puberty usually completes normally with recovery, but menarche is late ^[2]
Hypercholesterolaemia	Paradoxical — malnourished patients have HIGH cholesterol because: starvation → lipolysis → ↑ free fatty acids → hepatic cholesterol synthesis; also ↓ LDL receptor expression and ↓ cholesterol clearance ^[2]	Reversible with weight restoration
↑ Serum carotene (carotenodermia)	↑ Relative intake of carotene-rich vegetables (low-calorie foods) + ↓ metabolic clearance of carotene ^[2]	Reversible
Hypophosphataemia	Intracellular phosphate stores depleted in chronic starvation. Serum may appear normal until refeeding triggers precipitous intracellular shift. Exaggerated during refeeding ^[2]	Requires monitoring and supplementation, especially during refeeding
Dehydration	↓ Fluid intake + ↓ insensible water losses are balanced, but purging behaviours or diuretic misuse can cause overt dehydration ^[2]	Correct cautiously to avoid fluid overload
Electrolyte disturbances	HypoK⁺ (especially with vomiting or laxative/diuretic misuse), hypoNa⁺, hypoMg²⁺ ^[2]	Must be corrected urgently — hypoK⁺ is immediately life-threatening

Complication	Pathophysiology	Clinical Features
Delayed gastric emptying (gastroparesis)	↓ Autonomic tone (vagal dysfunction from starvation) + ↓ gut hormones → impaired gastric motility ^[2]	Bloating, nausea, fullness after eating, early satiety. This perpetuates the eating disorder — patients feel uncomfortably full after even small meals, which reinforces restriction
Decreased colonic motility	If chronic laxative misuse: damage to the myenteric plexus ("cathartic colon") → loss of intrinsic colonic motility ^[2]	Chronic constipation — paradoxically worsened by the laxatives that were supposed to treat it. Patients become dependent on laxatives for any bowel function
Acute gastric dilatation	Rare but potentially fatal. Occurs secondary to binge eating or excessive refeeding in a stomach with gastric atony ^[2]	Severe abdominal pain, distension, vomiting. Risk of gastric necrosis, perforation, death. This is why refeeding must be gradual
Superior mesenteric artery syndrome	Severe weight loss → loss of the mesenteric fat pad → the SMA compresses the third part of the duodenum between the SMA and the aorta	Postprandial vomiting, abdominal pain, early satiety. Diagnosed by CT angiography (reduced aortomesenteric angle). Resolves with weight restoration
Constipation	↓ Food volume → ↓ mechanical stimulation of peristalsis; also ↓ autonomic tone	Common; often misinterpreted by patients as evidence they "don't need to eat"

Complication	Pathophysiology	Clinical Significance
Normocytic normochromic anaemia	Starvation → gelatinous bone marrow transformation (normal haematopoietic marrow replaced by gelatinous mucopolysaccharide ground substance) → ↓ erythropoiesis ^[2]	Fatigue, pallor, exercise intolerance
Mild leucopenia with relative lymphocytosis	Same gelatinous marrow transformation → ↓ myelopoiesis. Lymphocytes are relatively spared because they are long-lived and less dependent on marrow turnover ^[2]	Neutropenia → ↑ infection risk. Alert criterion ^[2]. Infections may present atypically (blunted inflammatory response)
Thrombocytopenia	Same mechanism — ↓ megakaryocyte production in gelatinous marrow ^[2]	Bruising, bleeding risk. Usually mild

Why does the bone marrow become "gelatinous"? In severe starvation, the body catabolises the fat that normally fills the bone marrow cavity. This fat is replaced by a mucopolysaccharide-rich gelatinous matrix that is hostile to haematopoietic stem cells. All three cell lines are affected, producing a pancytopenia pattern. This is fully reversible with nutritional rehabilitation.

Complication	Pathophysiology	Clinical Significance
Osteopenia and osteoporosis	Multifactorial: (1) ↓ oestrogen → ↑ osteoclast activity (oestrogen normally suppresses RANKL and promotes OPG); (2) ↑ cortisol → ↓ osteoblast function; (3) ↓ IGF-1 → ↓ bone formation; (4) ↓ dietary calcium and vitamin D; (5) ↓ weight-bearing mechanical loading ^[2]	Can develop within 6–12 months of amenorrhoea. May be partially irreversible — peak bone mass may never be achieved if AN occurs during adolescence, leaving lifelong fracture risk. Pathological fractures can occur
Proximal myopathy	Protein catabolism → skeletal muscle wasting; also electrolyte derangement (hypoK⁺, hypoMg²⁺) → impaired muscle contraction ^[2]	Weakness — tested clinically with squat test (difficulty rising from squatting position) and sit-up test ^[2]
Stress fractures	Osteoporosis + excessive compulsive exercise	Common in exercising AN patients; may present atypically with minimal trauma

Osteoporosis in AN — A Potentially Irreversible Complication

Osteoporosis in AN is one of the few complications that may be permanently disabling. Adolescence is the critical window for achieving peak bone mass (which normally occurs by age ~25). If AN occurs during this window, peak bone mass may never be achieved, leaving the patient with lifelong increased fracture risk. Weight restoration is the only proven treatment — bisphosphonates are generally avoided in young women (teratogenic, very long half-life), and oestrogen replacement does NOT protect bone without concurrent weight restoration ^[2].

Complication	Pathophysiology	Reversibility
Cerebral atrophy	Starvation → loss of grey and white matter volume (neuronal loss, myelin breakdown)	Partially reversible with weight restoration — grey matter recovers more than white matter. Some cognitive deficits may persist
Cognitive impairment	Cerebral atrophy + hypoglycaemia + electrolyte disturbance → ↓ concentration, ↓ processing speed, ↓ executive function, ↓ set-shifting ability	Largely reversible but cognitive rigidity (a premorbid trait amplified by starvation) may persist
Peripheral neuropathy	Vitamin deficiency (B₁, B₆, B₁₂) from malnutrition	Reversible with supplementation and nutritional rehabilitation
Seizures	Hypoglycaemia, hypoNa⁺, hypoMg²⁺ — all lower the seizure threshold	Treat underlying electrolyte/metabolic cause

Complication	Pathophysiology
Lanugo hair	Compensatory mechanism for hypothermia — fine, downy hair on face, back, arms traps an insulating layer of air near the skin ^[2]
Dry skin	↓ Sebaceous gland activity from starvation; dehydration
Orange discolouration of palms and soles (carotenodermia)	↑ Serum carotene ^[2]
Hair thinning / alopecia	Protein malnutrition → telogen effluvium (premature shift of hair follicles to resting phase)
Acrocyanosis (blue/purple discolouration of extremities)	Peripheral vasoconstriction to preserve core temperature

Complication	Pathophysiology
Pre-renal AKI	Dehydration → ↓ renal perfusion → ↑ urea, ↑ creatinine
Chronic kidney disease	Chronic dehydration + chronic hypoK⁺ → hypokalemic nephropathy (vacuolar degeneration of renal tubular epithelial cells → impaired concentrating ability → nephrogenic diabetes insipidus-like picture)
Renal calculi	Chronic dehydration → concentrated urine → ↑ stone formation

These are complications directly caused by the compensatory behaviours — self-induced vomiting, laxative abuse, and diuretic misuse. They are the primary source of morbidity in BN (since BN patients are not typically in a starvation state) ^[2].

Complication	Pathophysiology	Clinical Finding
Electrolyte disturbances	Loss of HCl (H⁺ and Cl⁻) in gastric acid → metabolic alkalosis with compensatory renal K⁺ wasting → hypokalaemia + hypochloraemia ^[2]	HypoK⁺ → QT prolongation, muscle weakness, cardiac arrhythmia. The most dangerous acute complication
Parotid enlargement (sialadenosis)	Chronic stimulation of parotid glands by repeated vomiting → non-inflammatory hypertrophy (acinar cell enlargement). Bilateral, painless ^[2]	"Chipmunk facies" — bilateral parotid swelling giving a rounded facial appearance. ↑ Serum salivary amylase
Dental erosion (perimolysis)	Repeated exposure of dental enamel to gastric acid (pH ~1.5) → chemical dissolution of enamel, especially the palatal surfaces of upper incisors (directly bathed by vomitus) ^[2]	Sensitive teeth, dental caries, smooth-eroded enamel surfaces. Irreversible — enamel does not regenerate
Mallory-Weiss tear	Forceful retching → sudden ↑ intra-abdominal pressure → longitudinal mucosal tear at the gastro-oesophageal junction ^[2]	Haematemesis (bright red blood). Usually self-limiting but can cause significant haemorrhage
Oesophageal rupture (Boerhaave syndrome)	Extreme ↑ intra-oesophageal pressure during forceful vomiting → full-thickness oesophageal perforation	Surgical emergency — severe chest pain, subcutaneous emphysema, mediastinitis, sepsis. Rare but potentially fatal
GERD / Oesophagitis	Chronic acid exposure to oesophageal mucosa from repeated vomiting ^[2]	Heartburn, dysphagia. Long-term → Barrett's oesophagus → ↑ oesophageal adenocarcinoma risk
Epistaxis and subconjunctival haemorrhage	Forceful retching → ↑ venous pressure → rupture of small vessels in nasal mucosa and conjunctivae ^[2]	Nosebleeds, red eyes. Can be a clinical clue to secret purging
Russell's sign	Repeated trauma to the dorsum of the hand from teeth during self-induced vomiting (the hand is used to trigger the gag reflex) ^[2]	Calluses, scarring, abrasions on the knuckles (metacarpophalangeal joints). A pathognomonic sign
Aspiration pneumonia	Vomitus enters the trachea during self-induced vomiting	Cough, fever, dyspnoea. Chemical pneumonitis → bacterial superinfection
Metabolic alkalosis	Direct loss of HCl → ↑ serum HCO₃⁻ ^[2]	Blood gas: ↑ pH, ↑ HCO₃⁻, compensatory ↑ pCO₂

Complication	Pathophysiology	Clinical Finding
HypoNa⁺, hypoK⁺	Stimulant laxatives → ↑ intestinal secretion of water, Na⁺, K⁺ → osmotic diarrhoea with electrolyte losses ^[2]	Same dangers as vomiting-related hypoK⁺: cardiac arrhythmia, muscle weakness
Metabolic acidosis	Loss of bicarbonate-rich intestinal secretions (colonic bicarbonate loss) ^[2]	Contrast with vomiting → metabolic alkalosis. This is the distinguishing acid-base feature
Chronic constipation	Chronic stimulant laxative use → progressive damage to the myenteric plexus (Auerbach's plexus) → "cathartic colon" → loss of intrinsic colonic motility ^[2]	Paradoxically, the laxatives that were supposed to promote bowel function destroy the bowel's ability to function independently. Patients become laxative-dependent
Melanosis coli	Chronic stimulant laxative use (especially anthraquinone-based: senna, cascara) → lipofuscin deposition in colonic macrophages → brownish-black discolouration of colonic mucosa ^[2]	Seen on colonoscopy. Benign but a marker of chronic laxative abuse
Rectal prolapse	Chronic straining and ↓ pelvic floor muscle tone from repeated purgation	Protrusion of rectal mucosa through the anus
Steatorrhoea and malabsorption	Laxative-induced rapid transit → insufficient time for nutrient absorption	Weight loss (which paradoxically reinforces the behaviour), vitamin deficiencies

Complication	Pathophysiology
Dehydration	↑ Renal water excretion → volume depletion
HypoK⁺, hypoNa⁺	↑ Renal excretion of K⁺ and Na⁺ (mechanism depends on specific diuretic — loop diuretics waste K⁺ and Na⁺; thiazides waste K⁺ and Na⁺ and cause hypoCa²⁺ retention)
Pre-renal AKI	Volume depletion → ↓ renal perfusion
Pseudo-Bartter syndrome	Chronic diuretic/laxative abuse → chronic volume depletion → activation of the RAAS → ↑ aldosterone → when the purging stops, the elevated aldosterone causes avid Na⁺/water reabsorption → rebound oedema → patient panics, thinks they are "gaining weight," resumes purging. This is a significant barrier to treatment cessation

Pseudo-Bartter Syndrome — The Rebound Oedema Trap

When a patient with chronic purging stops vomiting or using diuretics/laxatives, they develop rebound oedema because chronic volume depletion has activated the RAAS (↑ renin, ↑ aldosterone). With cessation of purging, the kidneys avidly retain sodium and water → peripheral oedema and weight gain. This terrifies the patient, who may interpret the oedema as "getting fat" and resume purging. Clinicians must warn patients about this in advance and explain that the oedema is temporary (typically resolves within 1–2 weeks as RAAS activity normalises). Spironolactone can be used short-term to manage severe rebound oedema.

This was covered in detail in the management section but deserves emphasis here as a complication:

Feature	Detail
Definition	A potentially fatal constellation of metabolic derangements occurring upon nutritional reintroduction in severely malnourished patients ^[2]
Most characteristic finding	Hypophosphataemia — phosphate plummets as insulin drives it intracellularly for glycolysis and ATP synthesis ^[2]
Other electrolyte shifts	HypoK⁺, hypoMg²⁺ (same insulin-driven intracellular shift)
Fluid overload	Insulin → renal Na⁺/water retention → oedema → cardiac failure in a heart with ↓ muscle mass and ↓ compliance
Thiamine deficiency	↑ Glucose metabolism depletes thiamine stores → Wernicke's encephalopathy (confusion, ophthalmoplegia, ataxia) ^[2]
Clinical manifestations	Muscle weakness, seizures, peripheral oedema, cardiac dysrhythmias, hypotension, delirium ^[2]
Prevention	Thiamine supplementation BEFORE refeeding; start low go slow; daily PO₄/K⁺/Mg²⁺ monitoring; fluid restriction; prophylactic phosphate ^[2]
Risk group	BMI < 14, > 5 days of very low/absent caloric intake, pre-existing electrolyte disturbance

Distinct from cardiac failure: peripheral oedema (especially lower limbs) during early refeeding due to insulin-mediated Na⁺/water retention
Usually self-limiting; can be distressing to patients who interpret swelling as "getting fat"
Management: reassurance, leg elevation, mild Na⁺ restriction; avoid diuretics unless cardiac failure

Transaminase flare (↑ AST/ALT) during early refeeding
Mechanism: rapid carbohydrate provision → hepatic lipogenesis → steatosis → hepatocellular stress
Usually self-limiting; monitor and slow refeeding rate if transaminases rise dramatically

Complication	Pathophysiology	Prevalence
Depression	Multifactorial: starvation-related 5-HT/DA dysfunction, chronic social isolation, hopelessness, hypercortisolaemia. In BN, depression is very common but typically remits when BN is treated (suggesting it is secondary) ^[2]	AN: 75% lifetime prevalence ^[2]; BN: 50% ^[2]
Anxiety disorders (including OCD)	Premorbid trait amplified by starvation; shared serotonergic neurobiology ^[2]	High comorbidity, especially OCD
Deliberate self-harm	22% lifetime risk in AN ^[2]. Associated with comorbid depression, impulsivity (especially BN), emotional dysregulation	Significant — must be screened for
Suicide	Leading cause of death in AN (32%) ^[2]. Risk factors: chronic course, comorbid depression, substance abuse, social isolation	Extremely high — higher than depression alone
Substance abuse	BN especially associated with impulsivity → higher rates of alcohol/drug misuse ^[2]. AN binge-purge subtype also at elevated risk	BN > AN restricting type
Social withdrawal	Depression, food-related anxiety in social situations, shame, secrecy	Almost universal in severe cases
Labile mood, obsessional symptoms	Starvation amplifies premorbid obsessional and affective traits; 5-HT dysfunction ^[2]	Common during active illness; may improve with weight restoration

Sequela	Mechanism	Prognosis
Permanent short stature	If AN occurs pre-pubertally during the growth window → ↓ IGF-1 → irreversible growth impairment	Irreversible if growth plates have fused
Permanent osteoporosis	Failure to achieve peak bone mass during adolescence; chronic oestrogen deficiency and cortisol excess	May be partially irreversible — lifelong increased fracture risk
Fertility issues	Usually reversible with weight restoration, but prolonged amenorrhoea → may need assisted reproduction	Generally reversible
Dental damage	Enamel erosion from chronic vomiting is irreversible — requires dental restoration (crowns, veneers)	Irreversible
Cardiac damage	Prolonged starvation → myocardial fibrosis; may cause permanent ↓ cardiac function in severe cases	Partially reversible with weight restoration
Cognitive deficits	White matter changes may not fully recover	Partially reversible
Cathartic colon	Permanent damage to myenteric plexus from chronic laxative abuse → lifelong constipation	Irreversible
Chronic kidney disease	Chronic dehydration + chronic hypoK⁺ → hypokalemic nephropathy	May be irreversible

BED has a different complication profile because it lacks both starvation and purging:

Complication	Pathophysiology
Obesity	Recurrent binge eating without compensatory behaviours → chronic positive energy balance → weight gain
Metabolic syndrome	Obesity → insulin resistance, dyslipidaemia, hypertension, central adiposity
Type 2 diabetes mellitus	Insulin resistance from obesity → β-cell failure
Cardiovascular disease	Metabolic syndrome → atherosclerosis → MI, stroke
Obstructive sleep apnoea	Obesity → upper airway fat deposition → nocturnal airway collapse
Depression and low self-esteem	Shame about binge eating, weight stigma, perceived loss of control
Osteoarthritis	Mechanical loading from excess weight on weight-bearing joints

Mechanism	Key Complications	Most Dangerous
Starvation	Cardiac (bradycardia, QT prolongation, arrhythmia), endocrine (amenorrhoea, ↑ cortisol, hypoglycaemia), haematological (pancytopenia), skeletal (osteoporosis), neurological (cerebral atrophy), GI (gastroparesis)	Sudden cardiac death from arrhythmia; hypoglycaemic seizure/coma
Vomiting	Metabolic alkalosis, hypoK⁺, dental erosion, parotid enlargement, Mallory-Weiss tear, oesophageal rupture, aspiration pneumonia	Hypokalemic cardiac arrhythmia; Boerhaave syndrome
Laxatives	Metabolic acidosis, hypoK⁺/Na⁺, cathartic colon, melanosis coli	Hypokalemic cardiac arrhythmia
Diuretics	Dehydration, hypoK⁺/Na⁺, pre-renal AKI, pseudo-Bartter syndrome	Hypokalemic cardiac arrhythmia; AKI
Refeeding	Hypophosphataemia, hypoK⁺, hypoMg²⁺, fluid overload, Wernicke's encephalopathy	Cardiac failure; cardiac arrhythmia; Wernicke's
Binge eating (BED)	Obesity, metabolic syndrome, T2DM, CVD, OSA	Cardiovascular disease

High Yield Summary — Complications

AN has the highest mortality of ALL psychiatric disorders — SMR 23.14×; leading cause of death is suicide (32%), then starvation (19%), then cancer (11%).
Sudden cardiac death mechanism: Starvation + electrolyte depletion (hypoK⁺, hypoMg²⁺) → QT prolongation → torsades de pointes → VF → cardiac arrest.
BMI and organ failure: BMI 13.5–15 = all systems compromised; BMI 12–13.5 = organs begin to fail (marrow, muscle, heart); BMI < 12 = life-threatening.
Osteoporosis may be partially irreversible — failure to achieve peak bone mass during adolescent AN = lifelong fracture risk. Weight restoration (NOT HRT, NOT bisphosphonates) is the treatment.
Starvation endocrinopathy (↓ T3, ↓ LH/FSH, ↑ cortisol, ↑ GH/↓ IGF-1) is adaptive and reversible with refeeding — do NOT treat with hormone replacement.
Vomiting → metabolic alkalosis + hypoK⁺; laxatives → metabolic acidosis + hypoK⁺ — the acid-base difference is a classic exam question.
Refeeding syndrome: Hypophosphataemia is the hallmark; prevent with thiamine BEFORE refeeding, start low go slow, daily electrolyte monitoring.
Pseudo-Bartter syndrome: Chronic purging → RAAS activation → rebound oedema when purging stops → patient panics → resumes purging. Must warn patients in advance.
Dental erosion (perimolysis) from chronic vomiting is irreversible — enamel does not regenerate.
Depression comorbidity: 75% lifetime in AN, 50% in BN; in BN it often remits when the eating disorder is treated. Suicide risk is extremely high (22% lifetime DSH in AN).

Active Recall - Complications of Eating Disorders

References

^[2] Senior notes: ryanho-psych.md (Sections 9.1, 9.1.1, 9.1.2 — Eating Disorders: Physical features of AN, Abnormalities on investigation, BMI risk stratification, Clinical features of BN, Course and prognosis, Mortality, Refeeding syndrome, Complications)

High Yield Summary

Core psychopathology of all eating disorders: over-evaluation of weight and shape — self-worth = ability to control weight/shape/eating.
AN epidemiology: 3rd commonest chronic illness in teenage girls; F:M = 10:1; onset around menarche; highest mortality of ALL psychiatric disorders (SMR 23.14×); death from suicide (32%), starvation (19%), cancer (11%).
AN is ego-syntonic → poor insight; BN is ego-dystonic → better insight.
Aetiology = gene-environment interaction: 50–80% heritable; 12× risk in first-degree relatives; transmitted via temperamental traits (anxiety, perfectionism); precipitated by feeling "out of control" (puberty, life events).
Starvation physiology: HPG axis suppression → amenorrhoea; HPA activation → ↑ cortisol; ↓ T3 (sick euthyroid); bradycardia, hypotension, hypothermia; osteoporosis (↓ oestrogen + ↑ cortisol); gelatinous marrow → pancytopenia; hypercholesterolaemia (paradoxical); hypoglycaemia.
Purging: vomiting → metabolic alkalosis + hypoK⁺; laxatives → metabolic acidosis + hypoK⁺/Na⁺ — common exam trap!
BN vicious cycle: Strict diet → tension → craving → binge → guilt/disgust → purging → strict diet → repeat.
AN vs ARFID: Both have low weight + restriction. AN = fear of fatness/body image distortion. ARFID = no body image concern (sensory aversion, fear of choking, lack of interest).
Severity specifiers: AN = by BMI (mild ≥ 17, extreme < 15); BN = by compensatory behaviour frequency/week (mild 1–3, extreme ≥ 14).
Prognosis: Earlier treatment → better outcome. Adolescent AN with family-based treatment: 90% well at 5 years. Poor prognostic factors: late onset, long duration, personality problems, substance abuse.

High Yield Summary — Differential Diagnosis

The core psychopathology test (over-evaluation of weight and shape) is the single most important differentiator between eating disorders and their mimics.
Medical mimics of AN: Neoplasia (GI, hypothalamic, lymphoma), IBD, coeliac disease, hyperthyroidism, DM (including "diabulimia"), pituitary failure, chronic infection, Addison's disease, cystic fibrosis.
Psychiatric mimics: Depression (weight loss from anhedonia, no body image distortion), OCD (ego-dystonic obsessions not focused on weight/shape), social anxiety (fear of eating in public, not fear of fatness), BDD (preoccupation with specific body part, not overall weight/shape), psychosis (food refusal from delusions/hallucinations), substance use.
AN vs BN: Weight is the key — AN = significantly low weight; BN = normal weight. BN cannot be diagnosed during episodes of AN.
AN vs ARFID: Both have low weight and restriction. AN = fear of fatness + body image distortion. ARFID = sensory aversion, fear of choking, lack of interest, with NO body image concerns.
Red flags for medical mimic: Male patient, no body image distortion, patient distressed by weight loss, tachycardia, hyperkalaemia, focal neurological signs, atypical age.

High Yield Summary — Diagnosis and Investigations

AN diagnosis (DSM-5): Three criteria — (A) significantly low weight from energy restriction, (B) intense fear of weight gain OR persistent behaviour interfering with weight gain, (C) body image disturbance / undue influence of weight on self-evaluation / lack of recognition of seriousness. Subtypes: restricting vs binge-eating/purging. Severity by BMI (mild ≥ 17, extreme < 15).
BN diagnosis (DSM-5): Five criteria — (A) recurrent binge eating (large amount + loss of control), (B) recurrent compensatory behaviours, (C) ≥ 1/week for ≥ 3 months, (D) self-evaluation unduly influenced by weight/shape, (E) does not occur exclusively during AN. Severity by compensatory behaviour frequency/week.
BED vs BN: Both have binge eating; BED has NO compensatory behaviours.
AN vs ARFID: Both have low weight; AN has body image distortion / fat-phobia; ARFID does not.
DSM-5 removed amenorrhoea from AN criteria (but it still occurs clinically). DSM-5 added "persistent behaviour interfering with weight gain" to capture non-fat-phobic AN.
Key investigations and alert values: K⁺ < 3.0, PO₄ < 0.5, glucose < 2.5, HR < 40, QTc > 450 msec, BMI < 14, temperature < 35.5°C → urgent intervention / inpatient.
Starvation endocrinopathy: ↓ T3, ↓ LH/FSH/sex steroids, ↑ cortisol, ↑ GH / ↓ IGF-1 — all resolve with refeeding. Do NOT treat with hormones.
Vomiting → ↑ salivary amylase + metabolic alkalosis; laxatives → metabolic acidosis.
SCOFF mnemonic for screening: Sick, Control, One stone, Fat, Food.

High Yield Summary — Management

Setting of care: Inpatient if BMI ≤ 14 or physical complications (K⁺ < 2.5, HR < 40, arrhythmia, QTc > 450, glucose < 2.5). Day-patient if BMI 14–16 without complications. Outpatient if BMI > 16 without complications.
Four components: Medical complication management, nutritional rehabilitation, psychotherapy (mainstay), medications (adjunct only).
Refeeding syndrome: Caused by insulin surge driving phosphate/K⁺/Mg²⁺ intracellularly after carbohydrate reintroduction in starved patients. Most characteristic finding = hypophosphataemia. Prevention: thiamine BEFORE refeeding, start low go slow, daily electrolyte monitoring.
Adolescent AN: First-line = Maudsley Family Therapy (3 phases: weight restoration → returning control → healthy identity). Outcomes: 60% well at 1 year, 90% at 5 years.
Adult AN: First-line = CBT-E or MANTRA. Outcomes: 30% well at 1 year, 40–50% at 5 years.
BN: First-line = CBT-BN/CBT-E. First-line medication = fluoxetine 60 mg/day (NOT 20 mg).
BED: First-line = guided self-help / CBT-BED. FDA-approved medication = lisdexamfetamine.
Olanzapine is the most evidence-supported medication for AN (↑ appetite via anti-H₁, ↓ rumination, ↓ OC symptoms). Antidepressants have little evidence in acute AN.
Bupropion is CONTRAINDICATED in BN and AN (↓ seizure threshold + electrolyte disturbance = seizure risk).
SSRIs are ineffective in starving AN patients (↓ tryptophan → no substrate for SSRI to act on). Only consider after weight restoration.

High Yield Summary — Complications

AN has the highest mortality of ALL psychiatric disorders — SMR 23.14×; leading cause of death is suicide (32%), then starvation (19%), then cancer (11%).
Sudden cardiac death mechanism: Starvation + electrolyte depletion (hypoK⁺, hypoMg²⁺) → QT prolongation → torsades de pointes → VF → cardiac arrest.
BMI and organ failure: BMI 13.5–15 = all systems compromised; BMI 12–13.5 = organs begin to fail (marrow, muscle, heart); BMI < 12 = life-threatening.
Osteoporosis may be partially irreversible — failure to achieve peak bone mass during adolescent AN = lifelong fracture risk. Weight restoration (NOT HRT, NOT bisphosphonates) is the treatment.
Starvation endocrinopathy (↓ T3, ↓ LH/FSH, ↑ cortisol, ↑ GH/↓ IGF-1) is adaptive and reversible with refeeding — do NOT treat with hormone replacement.
Vomiting → metabolic alkalosis + hypoK⁺; laxatives → metabolic acidosis + hypoK⁺ — the acid-base difference is a classic exam question.
Refeeding syndrome: Hypophosphataemia is the hallmark; prevent with thiamine BEFORE refeeding, start low go slow, daily electrolyte monitoring.
Pseudo-Bartter syndrome: Chronic purging → RAAS activation → rebound oedema when purging stops → patient panics → resumes purging. Must warn patients in advance.
Dental erosion (perimolysis) from chronic vomiting is irreversible — enamel does not regenerate.
Depression comorbidity: 75% lifetime in AN, 50% in BN; in BN it often remits when the eating disorder is treated. Suicide risk is extremely high (22% lifetime DSH in AN).

Eating Disorders

1. Definition and Overview

2. Epidemiology

2.1 Anorexia Nervosa (AN)

2.2 Bulimia Nervosa (BN)

2.3 Binge Eating Disorder (BED)

2.4 Other Specified Feeding or Eating Disorders (OSFED)

3. Classification

Subtypes of AN (DSM-5)

Severity Specifiers

4. Anatomy and Function: Key Neurobiological Systems

4.1 Hypothalamic-Pituitary-Gonadal (HPG) Axis

4.2 Hypothalamic-Pituitary-Adrenal (HPA) Axis

4.3 Serotonin (5-HT) and Dopamine (DA) Systems

4.4 Appetite-Regulating Hormones

4.5 Reward and Interoception Circuits

5. Aetiology

5.1 Biological Factors

5.1.1 Genetics

5.1.2 Neurobiological Factors

5.1.3 Personality Traits

5.2 Psychological Factors

5.2.1 Cognitive Theories

5.2.2 Personal Factors

5.3 Family Factors

5.4 Societal Factors

5.5 Risk Factors for BN (Distinct from AN)

5.6 Precipitating Factors

6. Pathophysiology of Physical Complications

6.1 Starvation-Related Pathophysiology (Predominantly AN)

6.2 Purging-Related Pathophysiology (BN > AN binge-purge subtype)

7. Clinical Features

7.1 Anorexia Nervosa — Symptoms

A. Core Psychopathological Symptoms

B. Starvation-Related Symptoms

C. Behavioural Symptoms

7.2 Anorexia Nervosa — Signs

A. General Appearance

B. Cardiovascular Signs

C. GI Signs

D. Musculoskeletal

E. Neurological

F. Signs Specific to Purging Behaviour

7.3 Bulimia Nervosa — Symptoms

A. Core Psychopathological Symptoms

B. Binge Eating

C. Compensatory Behaviour

D. The Vicious Cycle of BN

E. Associated Psychiatric Symptoms

7.4 Bulimia Nervosa — Signs

7.5 Binge Eating Disorder — Clinical Features

7.6 Avoidant/Restrictive Food Intake Disorder (ARFID)

8. Approach to Assessment

8.1 History Taking Framework

8.2 Physical Examination

8.3 Investigations

9. Course and Prognosis

9.1 Anorexia Nervosa

9.2 Bulimia Nervosa

10. Summary Table: AN vs BN vs BED

Active Recall - Eating Disorders (Definition through Clinical Features)

References

1. Differential Diagnosis Framework

2. Medical Differential Diagnoses

3. Psychiatric Differential Diagnoses

4. Differentiating WITHIN Eating Disorders

5. Approach to Excluding Medical Differentials

6. Summary of Key Differentiating Principles

Active Recall - Differential Diagnosis of Eating Disorders

1. Diagnostic Criteria

1.1 Anorexia Nervosa — Diagnostic Criteria

DSM-5 Criteria [2]

ICD-10 Criteria (F50.0) [2]

1.2 Bulimia Nervosa — Diagnostic Criteria

DSM-5 Criteria [2]

ICD-10 Criteria (F50.2) [2]

1.3 Binge Eating Disorder — Diagnostic Criteria (DSM-5)

1.4 ARFID — Diagnostic Criteria (DSM-5)

1.5 OSFED — Examples (DSM-5) [2]

2. Diagnostic Algorithm