Behavioral Health

Eating disorders: anorexia nervosa diagnosis and management

Clinical Overview and When to Suspect Anorexia Nervosa

— Restricting type: weight loss via dieting, fasting, excessive exercise (no recurrent binge/purge in last 3 months)

— Binge-eating/purging type: recurrent binge eating or purging (vomiting, laxatives, diuretics, enemas)

— Lifetime prevalence ~0.6–1% females, ~0.3% males; peak onset adolescence to early adulthood

— Highest mortality of any psychiatric disorder (~5–10%), from cardiac arrhythmia, suicide, refeeding complications

— Adolescent/young adult with amenorrhea, weight loss, bradycardia, cold intolerance

— Athletes (gymnasts, runners, dancers, wrestlers) with stress fractures or fatigue

— Patient with type 1 diabetes who omits insulin for weight control (diabulimia, often AN/BN spectrum)

— Unexplained electrolyte derangements (hypokalemia, metabolic alkalosis if purging)

— Lanugo, parotid swelling, Russell sign (knuckle calluses)

Board pearl: AN can occur at any weight—"atypical anorexia nervosa" (in Other Specified Feeding/Eating Disorder) describes patients meeting all criteria except low BMI; the medical risks (bradycardia, electrolyte shifts, refeeding) are identical and should be managed the same way. Do not dismiss restrictive pathology because the BMI looks "normal."

Anorexia nervosa (AN) is a restrictive eating disorder defined by persistent energy intake restriction leading to significantly low body weight, intense fear of weight gain or behaviors that interfere with weight gain, and disturbance in body image or denial of seriousness of low weight.

DSM-5 subtypes:

Severity by BMI (adults): mild ≥17, moderate 16–16.99, severe 15–15.99, extreme <15 kg/m².

Epidemiology:

When to suspect on Step 3:

Screen with SCOFF questionnaire (≥2 positives suggests disorder): Sick, Control, One stone, Fat, Food.

Comorbidities: major depression, anxiety, OCD, substance use, type 1 diabetes, prior trauma.

Presentation Patterns and Key History

— Food rituals: cutting food into tiny pieces, eating very slowly, eliminating food groups, "clean eating," vegetarianism as a wedge

— Calorie counting, weighing food, hiding food, eating alone

— Exercise patterns: compulsive, driven, exercising while injured or ill, exercising in secret

— Purging behaviors: self-induced vomiting, laxative/diuretic abuse, diet pills, ipecac

— Body checking: repeated weighing, mirror checking, pinching

— Mood, anxiety, OCD traits (perfectionism, rigidity)

— Suicidal ideation, self-harm

— Trauma history, family conflict, peer or coach pressure

— Social media use (pro-ana content)

Key distinction: Anorexia vs bulimia nervosa—AN requires significantly low weight; bulimia nervosa occurs at normal or above-normal weight with recurrent binge–purge cycles ≥1×/week × 3 months. A purging AN patient who restores weight to normal but continues binge/purge may be reclassified as bulimia. Avoidant/Restrictive Food Intake Disorder (ARFID) lacks body-image disturbance and fear of weight gain—often sensory-based or fear of choking/vomiting; common in younger children and autism spectrum.

Chief complaints are often indirect: fatigue, syncope, amenorrhea, hair loss, cold hands, constipation, infertility evaluation, or stress fracture. Patients rarely volunteer restriction.

Behavioral history to elicit:

Weight history: premorbid weight, rate of loss, target weight, growth chart deviations in adolescents (crossing percentiles down is pathologic even before BMI cutoff).

Menstrual history: age of menarche, last period, secondary amenorrhea ≥3 months is a red flag.

Psychiatric/social screen:

Collateral history from parents/partners is essential; patients minimize.

Step 3 ambulatory framing: in a 17-year-old runner with 6 months amenorrhea and BMI 17, the right next step is not an MRI pituitary — it is a focused eating disorder history plus pregnancy test, TSH, prolactin, FSH/LH/estradiol, and CBC/CMP.

Physical Exam Findings and Hemodynamic Assessment

— Bradycardia <50 bpm awake (or <45 asleep): hallmark of severe AN from vagal tone and low T3

— Orthostatic hypotension: drop >20 mmHg systolic or >10 diastolic, or pulse rise >20

— Hypotension <90/60, hypothermia <35.6°C (96°F)

— Bradypnea, low oxygen consumption

— Lanugo (fine downy hair on back, cheeks, arms)

— Dry skin, carotenemia (orange palms from carotene-rich foods)

— Brittle hair, telogen effluvium (diffuse hair shedding)

— Acrocyanosis, cold extremities, poor capillary refill

— Parotid (sialadenosis) and submandibular gland enlargement—painless, bilateral, purging-related

— Dental erosion of lingual surfaces (perimylolysis), enamel loss → vomiting

— Angular cheilitis, glossitis

Step 3 management: Bradycardia in AN is not athletic conditioning—do not "reassure and follow up." HR <50 awake, orthostasis, hypotension <90/60, hypothermia <36°C, BMI <15, or weight <75% expected body weight are medical admission criteria. CCS move: place patient on continuous telemetry, warming blanket, slow IV/oral refeeding with phosphorus and thiamine, daily weights, and consult psychiatry.

Vital signs are the most actionable data point—a normal-appearing teen with HR 38 needs admission, not reassurance.

General: cachexia, sunken cheeks, prominent clavicles/ribs, sallow skin.

Skin/hair/nails:

Head/neck:

Hands: Russell sign—calluses/scars on dorsum of MCP from self-induced vomiting.

Cardiac: bradycardic, soft S1, possible mid-systolic click of mitral valve prolapse (from reduced LV mass).

Abdomen: scaphoid, may have epigastric tenderness, palpable stool (constipation), SMA syndrome if severely cachectic (postprandial vomiting, early satiety).

Neuro/MSK: proximal muscle weakness (squat test: inability to rise from squat without using hands), stress fracture tenderness, peripheral neuropathy.

GU: breast atrophy, vaginal dryness, delayed puberty in adolescents.

Diagnostic Workup — Initial Labs, ECG, and Bedside Studies

— CBC: leukopenia, anemia (normocytic), thrombocytopenia; pancytopenia from gelatinous marrow transformation

— CMP: hypokalemia, hyponatremia (water loading or SIADH), hypochloremic metabolic alkalosis (vomiting), non-anion-gap metabolic acidosis (laxatives), elevated BUN/creatinine (dehydration), low albumin late

— Magnesium, phosphorus, ionized calcium—baseline and serial; phosphorus is the refeeding lab

— Glucose: hypoglycemia in severe restriction (depleted glycogen)

— LFTs: transaminitis from starvation hepatitis or refeeding

— TSH, free T4: low-T3 (euthyroid sick) syndrome common—do not treat with levothyroxine

— Pregnancy test in all reproductive-age females

— LH, FSH, estradiol (hypogonadotropic hypogonadism); prolactin if galactorrhea

— Lipid panel: paradoxically elevated cholesterol

— Vitamin D, B12, folate, iron studies, zinc

— Urinalysis: low specific gravity (water loading) or high (dehydration), ketones

— Sinus bradycardia (most common)

— Prolonged QTc >450 ms (men) / >460 ms (women)—risk factor for torsades

— Low voltage, T-wave inversions, U waves (hypokalemia)

— ST changes

Board pearl: A QTc >500 ms, K <3.0, phosphorus <2.5, glucose <60, or HR <40 in an AN patient = ICU/step-down monitoring. Hypokalemia in AN is most often from purging, not restriction alone—if K is low and the patient denies purging, recheck the history and consider surreptitious diuretic or laxative use.

Goal: assess medical instability, identify electrolyte/refeeding risk, and exclude alternative diagnoses. Labs in AN are often deceptively normal in early restriction—severity is judged by vitals and trajectory, not labs alone.

Mandatory initial panel:

ECG in every patient:

DEXA scan: if amenorrhea >6 months or low weight >6 months—screen for osteopenia/osteoporosis.

Bedside: orthostatic vitals, weight in gown after voiding, height, BMI; for adolescents plot on growth chart.

Diagnostic Workup — Advanced and Confirmatory Studies

— Onset >40 years, male without classic body-image concerns

— Lymphadenopathy, fever, night sweats → malignancy, HIV, TB

— Diarrhea, bloody stools, oral ulcers → Crohn disease, celiac disease

— Hyperpigmentation, hypotension, hyponatremia + hyperkalemia → Addison disease

— Heat intolerance, tremor, tachycardia (not brady) → hyperthyroidism

— New neurologic findings or headaches → CNS lesion, hypothalamic tumor

— Celiac serology (tTG-IgA with total IgA), fecal calprotectin, colonoscopy

— HIV, RPR, TB testing

— AM cortisol, ACTH stimulation test for adrenal insufficiency

— MRI brain/pituitary if focal neuro deficits, visual field loss, diabetes insipidus, or panhypopituitarism pattern (low FSH/LH and low TSH and low cortisol)

— Upper GI series or CT for suspected SMA syndrome (postprandial vomiting in cachectic patient)

Key distinction: Both AN and panhypopituitarism cause amenorrhea + low gonadotropins, but AN has isolated hypogonadotropic hypogonadism with preserved or low-normal TSH and normal cortisol axis (cortisol may be mildly elevated from stress). Low TSH + low cortisol + low gonadotropins + bitemporal hemianopsia → image the pituitary.

Diagnosis of AN is clinical (DSM-5)—no confirmatory lab. Advanced studies are used to (1) exclude organic mimics when atypical, (2) quantify complications, and (3) guide refeeding.

When to broaden the workup (atypical features → look for organic disease):

Targeted studies when indicated:

DEXA (BMD): Z-score in premenopausal women / men <50; T-score otherwise. Repeat every 1–2 years if low weight persists.

Echocardiography: if murmur, heart failure signs, ipecac use (cardiomyopathy), or pre-refeeding in severe cases—look for pericardial effusion, reduced LV mass, mitral valve prolapse.

Resting energy expenditure (indirect calorimetry) used in specialized programs to guide caloric prescription; not required on boards.

Psychiatric assessment tools: Eating Disorder Examination (EDE), EDE-Q, EAT-26 for severity tracking.

Risk Stratification and First-Line Management Logic

— HR <50 bpm daytime (<45 at night) in adults; <50 in adolescents

— BP <90/60 or orthostatic ΔHR >20, ΔSBP >20

— Temperature <35.6°C (96°F)

— BMI <15 in adults; <75% median BMI for age/sex in adolescents

— Rapid weight loss (>1 kg/week sustained)

— K <3.0, Na <130, phosphorus <2.5, Mg <1.5, glucose <60

— QTc >500 ms or arrhythmia

— Syncope, seizure, dehydration unresponsive to oral intake

— Acute food refusal, suicidal ideation, psychosis

— Failure of outpatient treatment (no weight gain over weeks)

— Outpatient (weekly visits) → intensive outpatient (IOP) → partial hospitalization (PHP, ~6 hrs/day) → residential → inpatient medical → inpatient psychiatric

— Nutritional rehabilitation/weight restoration is the foundation—nothing works without it

— Psychotherapy (modality depends on age—see chunk 16)

— Medical monitoring of vitals, weight, electrolytes

— Family involvement (especially adolescents)

— Treat comorbid psychiatric disease

Step 3 management: The single most common Step 3 wrong answer is "start SSRI" or "start olanzapine" as first-line for AN. Wrong. First-line is nutritional rehabilitation + psychotherapy in a structured program. Medications are adjuncts and have no proven benefit in underweight AN.

Triage decision is the highest-yield Step 3 question. Use a structured rubric.

Indications for medical hospitalization (any one suffices):

Levels of care (least to most intensive):

Core treatment pillars (all levels):

Target weight: for adolescents, return to premorbid growth curve and resumption of menses; for adults, BMI ≥19–20 typically.

Caloric prescription: start low to avoid refeeding, advance daily. Typical: 1200–1500 kcal/day initially in malnourished inpatients, increase by 200–300 kcal every 1–2 days as tolerated; outpatients can often start higher (1500–1800).

Pharmacotherapy — Limited Role and Drug Choices

— Olanzapine (2.5–10 mg/day): modest evidence for weight gain and reduced obsessional thinking in adults with AN; consider in severe, treatment-resistant restrictive AN. Monitor metabolic side effects (less concerning when underweight).

— SSRIs (fluoxetine, sertraline): not effective for underweight AN; only after weight restoration may help comorbid depression/anxiety/OCD. Avoid bupropion—lowers seizure threshold in eating disorder patients (contraindicated).

— Mirtazapine: sometimes used for weight gain and insomnia/depression after restoration.

— Constipation: osmotic laxatives (polyethylene glycol); avoid stimulant laxatives (abuse risk).

— Gastroparesis/early satiety: metoclopramide cautiously (QT, EPS risk); small frequent meals.

— GERD: PPI.

— Osteoporosis:

▸ Adolescents: weight restoration is first-line; transdermal estradiol with cyclic progesterone improves BMD in adolescents with persistent amenorrhea

▸ Adults: bisphosphonates not first-line; avoid in reproductive-age women (teratogenic risk, long half-life). Use only in severe osteoporosis with fractures after multidisciplinary review.

▸ Oral contraceptives do NOT improve BMD in AN and may mask resumption of natural menses—avoid as a bone treatment.

— Vitamin D 800–2000 IU/day, calcium 1200–1500 mg/day.

— Thiamine 100 mg/day × 5–7 days before/during refeeding to prevent Wernicke encephalopathy.

— Multivitamin with zinc (zinc may modestly improve weight gain).

Board pearl: Bupropion is contraindicated in eating disorders (seizure risk). Oral contraceptives do not treat AN-related bone loss and may falsely reassure by inducing withdrawal bleeds—the right answer for a 19-year-old with AN amenorrhea is weight restoration, not OCPs.

Core principle: no medication has FDA approval or robust evidence for primary treatment of AN. Weight restoration alone reverses most psychiatric symptoms.

When medications are used—as adjuncts:

Treat specific comorbidities/complications:

QT-prolonging drug caution: avoid combinations (ondansetron + citalopram + olanzapine + hypokalemia = torsades).

Refeeding Protocol and Nutritional Rehabilitation

— Before first feed: check phosphorus, Mg, K, Ca, glucose, BUN/Cr; ECG; weight; orthostatics.

— Give thiamine 100 mg IV/PO ×5–7 days BEFORE and during refeeding (prevents Wernicke).

— Empirically replete phosphorus/Mg/K to high-normal before feeds if borderline.

— Start calories low: typically 1200–1500 kcal/day (or ~20 kcal/kg/day in highest-risk) PO if able; advance by 200–300 kcal every 1–2 days.

— Preferred route: oral whole foods ± oral supplements (Ensure, Boost). NG tube feeds if refusing or unable to meet goals. Avoid TPN unless gut nonfunctional.

— Daily labs ×5–7 days: phosphorus, Mg, K, Ca, glucose; daily weight (morning, post-void, gown); strict I/Os; continuous telemetry if HR <50 or QTc prolonged.

— Replete aggressively: phosphorus (oral K-phos/Na-phos or IV if <1.5 or symptomatic), Mg, K as needed.

— Target weight gain: 0.5–1 kg/week inpatient, 0.2–0.5 kg/week outpatient.

— Edema (refeeding edema)—reassure, restrict sodium, avoid diuretics unless heart failure

— CHF from rapid fluid/sodium loads in atrophic myocardium

— Hypoglycemia in first 72 hours

CCS pearl: On a CCS case of severe AN, your first three orders should be: (1) vitals + telemetry + ECG, (2) CBC, CMP, Mg, phos, ionized Ca, glucose, (3) thiamine 100 mg IV + multivitamin before any caloric load. Then write a structured refeeding diet order and daily electrolyte panels. Do not bolus IV fluids aggressively—volume overload kills the atrophied heart.

Refeeding syndrome is the central inpatient management hazard. Pathophysiology: starvation → intracellular depletion of phosphate, magnesium, potassium, thiamine; refeeding → insulin surge → cellular uptake of these ions → hypophosphatemia, hypomagnesemia, hypokalemia, thiamine deficiency → cardiac failure, arrhythmia, Wernicke, rhabdomyolysis, hemolysis, seizure.

High-risk features (any one): BMI <16, weight loss >15% in 3 months, little/no intake >10 days, low baseline electrolytes, alcohol/diuretic/insulin/chemo use.

CCS-style refeeding protocol:

Watch for:

Behavioral observation: supervised meals, bathroom locked or supervised ×60 min post-meal (prevent purging), no exercise initially.

Psychiatric/medical co-management with dietitian, therapist, social work, family.

Special Populations — Elderly and Renal/Hepatic Considerations

— Malignancy (GI, pancreatic, lung)

— Hyperthyroidism, Addison disease

— Depression with weight loss, dementia with feeding apraxia

— Medication side effects (SSRIs, stimulants, GLP-1 agonists)

— Lower baseline BMI thresholds for medical instability—an elderly patient with BMI 17 may be more unstable than a 19-year-old at the same BMI due to lower physiologic reserve.

— Osteoporosis is more severe and fracture risk higher; bisphosphonates more strongly indicated in older patients.

— Cardiac comorbidities lower the threshold for arrhythmia and heart failure during refeeding.

— Polypharmacy: review QT-prolonging meds (amiodarone, methadone, quinolones, ondansetron, antipsychotics).

— Pre-renal AKI is common from dehydration; rehydrate cautiously (volume overload risk).

— Chronic laxative/diuretic abuse → hypokalemic nephropathy, nephrocalcinosis.

— Adjust renally cleared drugs; avoid NSAIDs.

— Phosphate repletion: caution with IV phosphate in renal failure (hyperphosphatemia, hypocalcemia, calcium-phosphate precipitation).

— Starvation hepatitis: AST/ALT can rise to hundreds or thousands; resolves with refeeding.

— Refeeding hepatitis: transaminases rise after starting feeds—usually self-limited; monitor.

— Synthetic dysfunction (low albumin, INR elevation) in severe malnutrition.

— Avoid hepatotoxic drugs (acetaminophen dosing reduced; avoid valproate).

Key distinction: Starvation transaminitis (severely underweight, pre-refeeding) typically reflects autophagy/hepatocyte injury and improves with refeeding; refeeding transaminitis (rises 1–3 weeks after feeds start) reflects hepatic steatosis from carbohydrate load and improves with slower advancement. Either way, the answer is rarely "stop feeds"—it is "continue refeeding carefully and monitor."

Late-onset AN (>40 years): less common but real; often relapse of adolescent illness or new onset triggered by life stressors (divorce, bereavement, illness). Always rule out organic mimics first:

Geriatric pitfalls:

Renal impairment:

Hepatic dysfunction:

Special Populations — Adolescents, Pregnancy, Athletes, Males

— Use % median BMI for age/sex, not adult BMI cutoffs. <75% median BMI = severe.

— Growth curve deviation (crossing percentiles down) is pathologic regardless of absolute BMI.

— Family-Based Treatment (FBT, Maudsley method) is first-line psychotherapy—parents take charge of refeeding initially, then gradually return autonomy. Strongest evidence for outpatient AN.

— Pubertal delay, primary amenorrhea, height stunting; weight restoration may allow catch-up growth if early.

— Pediatric admission criteria are stricter (HR <50 day/<45 night, BMI <75% median, electrolyte abnormality, orthostasis).

— AN reduces fertility (anovulation), but patients can conceive even with amenorrhea—counsel on contraception.

— Pregnancy in active AN → IUGR, preterm birth, miscarriage, low birth weight, postpartum depression, hyperemesis worsening illness.

— Multidisciplinary care: OB, psychiatry, nutrition, MFM.

— Avoid teratogens: valproate, topiramate (also weight-loss promoting—double bad).

— Monitor weight gain against IOM targets; underweight women should gain 12.5–18 kg.

— Triad: low energy availability, menstrual dysfunction, low BMD.

— RED-S broader: also affects cardiovascular, metabolic, GI, immune, psychological health, and applies to males.

— Stress fractures (especially femoral neck, tibia, metatarsals) are red flags.

— Management: increase caloric intake, decrease training volume, treat eating disorder.

— Often missed; present with muscularity concerns (muscle dysmorphia), excessive exercise, anabolic steroid use.

— Low testosterone, decreased libido, ED, reduced BMD.

— Higher mortality, possibly from delayed diagnosis.

Board pearl: For an adolescent with AN, the best-evidenced outpatient psychotherapy is FBT (Maudsley), not individual CBT. For adults, CBT-E (enhanced CBT) is first-line.

Adolescents:

Pregnancy:

Athletes — Female Athlete Triad / RED-S (Relative Energy Deficiency in Sport):

Males (~10–25% of cases):

Complications and Adverse Outcomes

— Sinus bradycardia, hypotension, orthostasis

— QT prolongation → torsades de pointes, sudden cardiac death

— Reduced LV mass, pericardial effusion, mitral valve prolapse

— Refeeding-induced CHF (atrophic myocardium + fluid load)

— Ipecac cardiomyopathy (irreversible) from chronic ipecac abuse

— Hypogonadotropic hypogonadism, amenorrhea, infertility

— Low-T3 (euthyroid sick) syndrome—do NOT treat with levothyroxine

— Hypoglycemia, hypercortisolism (functional), hypercholesterolemia

— Osteopenia/osteoporosis, stress fractures

— Growth retardation in adolescents

— Constipation, delayed gastric emptying, GERD

— Mallory-Weiss tears, esophagitis, esophageal rupture (purging)

— Superior mesenteric artery (SMA) syndrome—loss of mesenteric fat pad → duodenal compression → postprandial vomiting; treated with refeeding (paradoxically requires eating despite vomiting; sometimes NJ tube past obstruction)

— Acute gastric dilatation with rapid refeeding → necrosis/perforation (rare)

— Hepatic steatosis, transaminitis

— Gelatinous marrow transformation → pancytopenia, reversible with refeeding

— Iron, B12, folate deficiencies

— Cognitive impairment, cortical atrophy ("pseudoatrophy"—largely reversible)

— Seizures (hyponatremia, hypoglycemia)

— Peripheral neuropathy

— Wernicke encephalopathy if refed without thiamine

— Major depression, anxiety, OCD, suicide (second leading cause of death)

Key distinction: Refeeding hypophosphatemia is the dangerous early refeeding complication (days 1–7) → cardiac failure, respiratory failure, rhabdomyolysis, hemolysis, seizure, delirium. Refeeding edema is a later, benign complication (week 2–3) → reassure, restrict sodium, do not diurese.

Cardiovascular (leading cause of death):

Endocrine/metabolic:

GI:

Hematologic:

Renal: pre-renal AKI, hypokalemic nephropathy, nephrolithiasis

Neuro/psych:

Dermatologic: lanugo, carotenemia, dry skin, acrocyanosis

Dental: enamel erosion, caries, parotid hypertrophy (purging)

When to Escalate Care — ICU, Consults, and Transfer

— HR <40 bpm or symptomatic bradycardia

— SBP <80 or symptomatic orthostasis unresponsive to fluids

— QTc >500 ms or any arrhythmia

— Phosphorus <1.5 mg/dL during refeeding, regardless of symptoms

— K <2.5, Na <125, glucose <50, Mg <1.0

— Altered mental status, seizure, suspected Wernicke

— Acute heart failure (refeeding-induced)

— Hemodynamic instability after syncope, fall, or aspiration

— Psychiatry / eating disorder team — diagnosis, level-of-care recommendation, comorbidity treatment

— Registered dietitian — caloric prescription and meal planning

— Adolescent medicine or internal medicine — medical co-management

— Cardiology — persistent bradyarrhythmia, QT >500, suspected cardiomyopathy

— Endocrinology — severe osteoporosis, persistent amenorrhea after restoration, pituitary concerns

— GI — SMA syndrome, severe gastroparesis, hepatic dysfunction

— Social work — disposition, school/work coordination, insurance authorization for residential

— Ethics consult — refusal of life-saving treatment, capacity questions

— Facility cannot provide specialized eating disorder care + medical stabilization

— Need for residential treatment after medical clearance

— Pediatric patient at adult facility (transfer to pediatric eating disorder unit)

— HR ≥45 awake, normothermia, normal orthostatics

— Electrolytes stable off IV repletion

— Eating ≥75% of prescribed meals voluntarily

— Plan for next level of care (PHP/IOP/outpatient) in place before discharge

— Psychiatric stability (no active SI)

CCS pearl: A common Step 3 CCS pitfall is discharging the AN patient as soon as electrolytes normalize but before outpatient/PHP follow-up is arranged. The right move is to delay discharge until the transition is booked—relapse and re-admission rates are highest in the first 30 days post-discharge.

ICU/step-down telemetry criteria:

Multidisciplinary consults to place early:

Transfer indications:

Discharge from acute medical hospitalization (minimum criteria):

Key Differentials — Other Eating and Feeding Disorders

— Recurrent binge eating + compensatory behaviors (vomiting, laxatives, fasting, excessive exercise) ≥1×/week × 3 months

— Weight typically normal or above normal (key distinction from purging-type AN)

— Similar medical complications: hypokalemia, Mallory-Weiss tears, parotid hypertrophy, Russell sign, dental erosion

— First-line treatment: CBT-E + fluoxetine 60 mg/day (only FDA-approved drug for an eating disorder); avoid bupropion

— Recurrent binge eating without compensation, ≥1×/week × 3 months, marked distress

— Most common eating disorder in US; associated with obesity

— Treatment: CBT, IPT (first-line); lisdexamfetamine (Vyvanse) is FDA-approved; SSRIs and topiramate are options

— Restricted intake → weight loss/nutritional deficiency, but no body-image disturbance and no fear of weight gain

— Sensory aversion, fear of choking/vomiting, lack of interest in food

— Common in children, autism spectrum; can persist into adulthood

— Treatment: feeding therapy, CBT-AR, exposure therapy

— All AN criteria met except low BMI

— Same medical risks; treat the same way—do not be falsely reassured by "normal" weight

Key distinction: AN vs purging-type BN — both can binge and purge. The discriminator is weight: AN = significantly low; BN = normal or higher. AN vs ARFID — both restrict and lose weight. The discriminator is body-image disturbance and fear of weight gain (present in AN, absent in ARFID).

Bulimia nervosa (BN):

Binge-Eating Disorder (BED):

Avoidant/Restrictive Food Intake Disorder (ARFID):

Pica: eating non-nutritive substances (ice, dirt, paper) ≥1 month; rule out iron-deficiency anemia, pregnancy, intellectual disability, schizophrenia.

Rumination disorder: repeated regurgitation/re-chewing without GI cause.

Atypical anorexia nervosa (Other Specified Feeding/Eating Disorder, OSFED):

Night-eating syndrome, purging disorder (purging without binge), orthorexia (not in DSM-5 but clinically relevant)

Key Differentials — Medical and Psychiatric Mimics

— Hyperthyroidism: weight loss + increased appetite, tachycardia, tremor, heat intolerance, ↓TSH/↑T4. Distinguishes from AN (which has low T3, normal/low TSH, bradycardia, cold intolerance).

— Type 1 diabetes (new onset): polyuria, polydipsia, hyperglycemia, DKA risk. Consider in any adolescent with rapid weight loss.

— Addison disease: weight loss, hyperpigmentation, hypotension, hyponatremia + hyperkalemia, low cortisol.

— Pheochromocytoma, hyperparathyroidism (rarely)

— Celiac disease: diarrhea, bloating, weight loss; tTG-IgA positive; iron deficiency

— Inflammatory bowel disease (Crohn): diarrhea, abdominal pain, perianal disease, fevers; ↑ESR/CRP, fecal calprotectin

— Chronic pancreatitis, malabsorption

— Achalasia, peptic ulcer, gastroparesis

— Major depression with poor appetite — weight loss is unintentional; no body image distortion, no fear of weight gain

— OCD with contamination fears of food

— Schizophrenia with delusions about food being poisoned

— Substance use (stimulants → appetite suppression)

— Somatic symptom disorder, conversion disorder

Board pearl: The single most useful history question to distinguish AN from medical/depressive weight loss is: "Are you trying to lose weight?" AN patients fear weight gain and pursue weight loss; depression and medical illness produce unintentional weight loss without body-image disturbance. A 19-year-old with weight loss who wants to gain weight back but cannot eat is not AN—keep looking for organic disease.

Endocrine causes of weight loss:

GI causes:

Malignancy: lymphoma, GI cancers, lung cancer—B symptoms, lymphadenopathy, abnormal CBC.

Infection: HIV, TB, chronic hepatitis, parasitic infection in returning traveler.

Psychiatric mimics:

Medications: stimulants, SSRIs (early), metformin, GLP-1 agonists (semaglutide), topiramate, bupropion, chemotherapy, levothyroxine excess.

Other: anorexia of aging, dementia (feeding apraxia), heart failure cachexia, COPD cachexia.

Secondary Prevention, Discharge Plan, and Long-Term Management

— Multivitamin with iron and zinc daily

— Vitamin D 800–2000 IU/day, calcium 1200–1500 mg/day

— PPI if GERD/esophagitis from purging

— Polyethylene glycol for constipation

— SSRI (fluoxetine, sertraline) only if comorbid depression/anxiety/OCD persists after weight restoration

— Olanzapine 2.5–10 mg if severe restrictive AN with persistent obsessional eating thoughts and inadequate weight gain

— Avoid bupropion (seizure risk), avoid stimulants, avoid OCPs as bone treatment

— Outpatient eating disorder team booked within 1 week

— Weight, vitals, and electrolyte plan documented

— Caregiver/family education and meal supervision plan

— Crisis plan and 24-hour psychiatric contact

— School/work accommodations (504 plan, FMLA, work note)

— Insurance authorization for ongoing PHP/IOP

— Weekly weights with pre-set weight floor; if drops below, re-escalate care

— Therapy: FBT for adolescents, CBT-E for adults; consider DBT for emotion dysregulation, ACT, IPT

— Dietitian visits weekly to monthly

— Medical follow-up every 1–4 weeks initially, then every 3 months

— Annual DEXA if BMD low or persistent amenorrhea; q2y otherwise during illness

— Dental follow-up if purging history

— Address comorbid substance use, trauma

— Identify triggers (transitions: college, breakup, bereavement, pregnancy, sports season)

— Weight floors and "check-in" criteria

— Family education on warning signs (food rituals, exercise creep, weighing, body checking)

— Pregnancy planning before conception in women with prior AN

Step 3 management: Outcomes correlate with early intervention and duration of illness. ~50% achieve full recovery, 30% partial, 20% chronic; mortality ~5–10% over decades. The first 12 months after weight restoration is the highest-risk relapse window—maintain therapy and follow-up intensity even when the patient "looks fine."

Discharge medication list (typical):

Discharge requirements ("never discharge without"):

Long-term outpatient plan:

Relapse prevention:

Follow-Up, Monitoring, and Psychotherapy Modalities

— Weekly weights at outpatient visits—gowned, post-void, same scale, blind weights often used

— Vitals (HR, BP, orthostatics, temperature) at each visit early

— Weight gain target: 0.2–0.5 kg/week outpatient, 0.5–1 kg/week PHP/inpatient

— During active refeeding (inpatient): phos/Mg/K/Ca/glucose daily ×5–7 days

— Stable outpatient: CMP, Mg, phos every 1–3 months while underweight; CBC, TSH, lipids, vitamin D, B12 every 3–6 months

— ECG if QTc was prolonged, electrolytes shift, or new symptoms

— DEXA every 1–2 years while underweight or amenorrheic

— Pregnancy test before any imaging/medication in reproductive-age women

— Adolescents: Family-Based Treatment (FBT, Maudsley) is first-line. Three phases: (1) parents take charge of refeeding, (2) gradual return of eating autonomy, (3) adolescent identity work. Strongest evidence base.

— Adults: Enhanced CBT (CBT-E) is first-line. 20–40 sessions. Addresses overvaluation of shape/weight, dietary restraint, mood intolerance, interpersonal triggers, perfectionism.

— Alternatives: MANTRA (Maudsley Anorexia Nervosa Treatment for Adults), SSCM (Specialist Supportive Clinical Management), psychodynamic therapy, IPT, DBT for affect dysregulation.

— Restricted during weight restoration

— Gradually reintroduced based on weight, vitals, mental state, and orthopedic clearance

— Avoid solo, compulsive, or high-volume exercise; supervised structured activity preferred

— Move from prescribed meal plans toward intuitive eating as recovery progresses

— Address food fears and "fear foods" through graded exposure

Board pearl: Return of spontaneous menses within ~6 months of reaching target weight is the best clinical marker of physiologic recovery; persistent amenorrhea at goal weight suggests inadequate energy availability (hidden restriction or excessive exercise)—recheck the food and exercise log, do not jump to OCPs.

Vital sign and weight monitoring:

Lab monitoring:

Resumption of menses is a key biomarker of recovery—often requires 90–95% of expected body weight.

Psychotherapy by age:

Exercise:

Nutritional counseling:

Ethical, Legal, and Patient Safety Considerations

— AN is unique among psychiatric disorders—patients often have preserved cognitive capacity for most decisions but impaired capacity specifically around food and weight due to ego-syntonic illness.

— Severe AN with imminent medical risk (HR <40, K <2.5, refusing all intake) may warrant involuntary hospitalization under state mental health holds.

— Forced feeding (NG tube under restraint) is ethically and legally complex—reserved for life-threatening cases when capacity is impaired and patient/family disagree. Requires ethics consultation and clear documentation.

— In adolescents, parental consent generally suffices; in adults, two-physician psychiatric hold or court-ordered treatment may be required.

— Adolescents: in most US states, eating disorders fall under general medical care; parents must be informed for safety.

— Disclose to family/caregivers if imminent danger (suicidal ideation, refusal of life-saving treatment).

— Child abuse/neglect if parents knowingly withhold treatment from a medically unstable minor → report to CPS.

— Coach- or trainer-induced restriction in minors may warrant institutional reporting.

— Highest relapse and mortality risk in the 30 days after inpatient discharge.

— Do not discharge without confirmed outpatient appointment, dietitian, therapist, and warm handoff.

— Pediatric → adult care transition (age 18–25) is another vulnerable window—proactively bridge.

— Mental health parity laws require eating disorder coverage; document medical necessity carefully (vitals, BMI, electrolytes) to support PHP/residential authorization.

— Bathroom locks/supervision (purging risk), no exercise without staff knowledge, search of belongings if hidden laxatives/diet pills suspected, blind weights, supervised meals.

— Suicide precautions if SI present; remove access to means.

Step 3 management: Forced NG feeding of a competent adult AN patient refusing care is not automatic—the right answer on boards is usually (1) re-assess capacity specifically regarding food/weight, (2) ethics consultation, (3) involve family and psychiatry, (4) consider involuntary hold if imminent life-threat, rather than immediate physical restraint.

Capacity and involuntary treatment:

Confidentiality limits:

Mandatory reporting:

Transitions of care (high-yield Step 3 safety theme):

Insurance and access:

Patient safety on the unit:

Athletes/military/performers: sport governing bodies require medical clearance—do not clear an athlete with active medical instability regardless of pressure.

High-Yield Associations and Rapid-Fire Clinical Facts

Board pearl: When you see a stem with "competitive runner, stress fracture, missed periods for 8 months, BMI 18.5"—do not be distracted by the "normal" BMI. The diagnosis is Female Athlete Triad / atypical AN / RED-S, and the management is increase calories, decrease training, treat eating disorder—not OCPs and not bisphosphonates.

Highest mortality of any psychiatric disorder (~5–10% lifetime); causes: cardiac arrhythmia, refeeding complications, suicide.

Bradycardia + hypothermia + amenorrhea + lanugo in a teenage girl = AN until proven otherwise.

Phosphorus is THE refeeding lab. Check daily, replete aggressively, never start feeds without thiamine.

Thiamine before glucose in any malnourished patient—prevents Wernicke encephalopathy (ataxia, ophthalmoplegia, confusion) and Korsakoff syndrome (anterograde amnesia, confabulation).

Russell sign = knuckle calluses from self-induced vomiting → purging behavior.

Parotid hypertrophy + dental erosion (lingual surfaces) = chronic vomiting.

Hypokalemia + metabolic alkalosis → vomiting or diuretic abuse. Non-anion-gap metabolic acidosis → laxative abuse.

Low T3, low/normal TSH, normal T4 = euthyroid sick syndrome → do NOT give levothyroxine.

Hypogonadotropic hypogonadism (low FSH/LH/estradiol) = functional from low energy availability → reverses with weight gain.

DEXA for any AN patient with amenorrhea or low weight >6 months.

First-line psychotherapy: FBT for adolescents, CBT-E for adults.

First-line treatment for AN overall: nutritional rehabilitation + psychotherapy, NOT medications.

Fluoxetine 60 mg is FDA-approved for bulimia nervosa (NOT AN). Lisdexamfetamine is FDA-approved for binge-eating disorder.

Bupropion contraindicated in eating disorders.

OCPs do not improve BMD in AN—do not use as a bone treatment.

Olanzapine modestly helps weight gain in severe AN adults.

SMA syndrome in cachectic patient → postprandial vomiting → treat with refeeding (sometimes NJ tube past Treitz).

Gelatinous marrow transformation → pancytopenia, reverses with weight gain.

Pseudoatrophy (cortical) on MRI in AN → reversible.

Female Athlete Triad = low energy availability + menstrual dysfunction + low BMD; RED-S is the broader, male-inclusive concept.

Board Question Stem Patterns

Step 3 management: When the stem gives you bradycardia + orthostasis + BMI <15 in an AN patient, the answer is always admit, never "reassure and outpatient follow-up."

Classic vignette 1 — Diagnosis: 16-year-old girl brought by mother for amenorrhea ×8 months. Runs 8 miles/day, eats only "clean foods," BMI 16, HR 42, BP 88/55, lanugo on forearms. Best next step? → Hospital admission for medical stabilization (HR <50 + BMI <16 + orthostasis).

Classic vignette 2 — Refeeding: Inpatient with severe AN started on 2500 kcal/day. Day 3: confused, tachypneic, weak. Phos 1.2, Mg 1.1, K 2.8. Diagnosis? → Refeeding syndrome. Management: slow feeds, replete phos/Mg/K, give thiamine, telemetry.

Classic vignette 3 — Pharmacotherapy: 22-year-old with AN, BMI 15.5, restored care, asks about an antidepressant. Best answer? → Nutritional rehabilitation first; SSRIs ineffective until weight restored. Avoid bupropion.

Classic vignette 4 — Bone health: 20-year-old with AN, amenorrhea ×2 years, DEXA Z-score –2.5. Best treatment? → Weight restoration (first-line); calcium + vitamin D; NOT OCPs, NOT bisphosphonates first-line in reproductive-age woman.

Classic vignette 5 — Differential: 17-year-old with weight loss, diarrhea, bloating, iron-deficiency anemia, BMI 17 — wants to gain weight but cannot. Diagnosis? → Celiac disease (check tTG-IgA), not AN.

Classic vignette 6 — Psychotherapy: 14-year-old with AN, medically stable, BMI 17.5. Best psychotherapy? → Family-Based Treatment (FBT/Maudsley).

Classic vignette 7 — Adult psychotherapy: 28-year-old with AN, restored, residual food fears. Best therapy? → CBT-E.

Classic vignette 8 — Bulimia: 19-year-old, BMI 22, binges + vomits ×5/week, hypokalemia, parotid swelling. Diagnosis? → Bulimia nervosa. Treatment: CBT + fluoxetine 60 mg.

Classic vignette 9 — Athletic: Female collegiate runner with multiple stress fractures, amenorrhea, BMI 19. Diagnosis? → Female Athlete Triad / RED-S. Management: increase calories, decrease training.

Classic vignette 10 — Capacity: AN patient, BMI 12, K 2.3, refuses NG feeds, "lucid" otherwise. Best step? → Re-assess decision-specific capacity, ethics consult, involuntary psychiatric hold if criteria met.

Classic vignette 11 — Thyroid: AN patient with TSH 0.8, free T4 0.9, T3 low. Action? → Do nothing—euthyroid sick syndrome.

One-Line Recap

Anorexia nervosa is a high-mortality restrictive eating disorder whose first-line treatment is nutritional rehabilitation and psychotherapy (FBT for adolescents, CBT-E for adults), with medical hospitalization indicated for bradycardia, electrolyte derangement, or low BMI, and where the dominant inpatient hazards are refeeding syndrome and cardiac arrhythmia—prevented by slow caloric advancement, daily phosphorus monitoring, and prophylactic thiamine.

Board pearl: If you remember only three things — (1) weight restoration is the treatment, (2) thiamine before glucose, phosphorus is the refeeding lab, and (3) FBT for adolescents, CBT-E for adults — you will answer the majority of Step 3 anorexia nervosa questions correctly.

Diagnosis is clinical (DSM-5): restriction → significantly low weight + fear of weight gain + body-image disturbance. Severity by BMI; atypical AN has all features at normal BMI.

Admit for: HR <50, BP <90/60, BMI <15 (or <75% median in adolescents), K <3.0, phos <2.5, QTc >500, hypothermia, syncope, suicidality, or outpatient failure.

Refeeding rules: thiamine before glucose, start low (1200–1500 kcal/day), advance 200–300 kcal q1–2 days, daily phos/Mg/K ×5–7 days, telemetry, supervised meals, no diuretics for refeeding edema.

Medications are adjuncts only: olanzapine for severe AN; SSRIs after weight restoration for comorbid mood/anxiety; bupropion contraindicated; OCPs do not treat bone loss; fluoxetine 60 mg is for bulimia, not AN; lisdexamfetamine is for binge-eating disorder.

Long-term: highest mortality of any psychiatric disorder (~5–10%); leading causes are cardiac arrhythmia and suicide; relapse risk peaks in the first year post-restoration—maintain dietitian + therapist + medical follow-up + DEXA monitoring, and guard the discharge transition with a confirmed warm handoff before the patient leaves the hospital.