Behavioral Health

Eating disorders: bulimia nervosa diagnosis and management

Clinical Overview and When to Suspect Bulimia Nervosa

— Recurrent episodes of binge eating (eating, in a discrete period, an amount definitively larger than most would eat, with a sense of loss of control)

— Recurrent inappropriate compensatory behaviors: self-induced vomiting, laxatives, diuretics, enemas, fasting, excessive exercise

— Frequency: ≥1 episode/week for ≥3 months

— Self-evaluation unduly influenced by body shape and weight

— Does NOT occur exclusively during episodes of anorexia nervosa

— Young adult with dental erosion, parotid swelling, or Russell sign (knuckle calluses) on routine visit

— Unexplained hypokalemia, metabolic alkalosis, or recurrent esophagitis/Mallory-Weiss tears

— Patient requesting laxatives, diuretics, or weight-loss medications repeatedly

— Adolescent with normal BMI but secretive eating, frequent bathroom visits after meals, or fluctuating weight

Board pearl: BMI in bulimia nervosa is typically ≥18.5. If the patient is underweight AND binging/purging, the diagnosis is anorexia nervosa, binge-eating/purging type, not BN — this distinction drives treatment intensity and prognosis.

Bulimia nervosa (BN) is a disorder of recurrent binge eating coupled with compensatory behaviors aimed at preventing weight gain, occurring in individuals whose weight is typically normal or overweight — a key feature that distinguishes it from anorexia nervosa binge-purge subtype.

DSM-5 core criteria (must remember verbatim for boards):

Epidemiology: lifetime prevalence ~1–1.5% in women, ~0.5% in men; onset typically late adolescence to young adulthood; higher rates in athletes (wrestlers, gymnasts, dancers, jockeys), models, and individuals with T1DM (where insulin omission becomes a purging behavior = "diabulimia").

When to suspect on Step 3:

Comorbidity is the rule, not the exception: major depression (~70%), anxiety disorders, PTSD, borderline personality, substance use disorder (especially stimulants/alcohol).

Presentation Patterns and Key History

— Binge episodes: trigger (negative affect, dietary restriction, interpersonal stress), foods consumed (typically high-calorie, "forbidden" foods), duration (usually <2 hours), feeling of loss of control

— Compensatory behaviors: method (vomiting most common ~80–90%; laxatives ~30%; diuretics; fasting; compulsive exercise), frequency, duration

— Weight history: cycling, prior dieting, family weight focus

— Body image: overvaluation of weight/shape in self-worth — ask directly: "How much does your weight or shape affect how you feel about yourself?"

— Sick: make yourself sick because uncomfortably full?

— Control: worry you've lost control over eating?

— One stone (14 lb) lost in 3 months?

— Fat: believe you're fat when others say thin?

— Food: would you say food dominates your life?

Key distinction: Binge-eating disorder (BED) has binges WITHOUT compensatory behaviors and is the most common eating disorder in the US — patients are typically overweight/obese. BN has the binge + purge cycle; BED is binges alone. Treatment overlaps (CBT, SSRIs, lisdexamfetamine is FDA-approved for BED but NOT BN).

Step 3 management: When a vignette describes recurrent vomiting in a normal-BMI woman with dental erosions, screen with SCOFF first, then proceed to full diagnostic interview — do not order extensive GI workup before psychiatric assessment.

Patients rarely volunteer the diagnosis — shame and secrecy are core features. Step 3 vignettes embed the diagnosis in chief complaints like "fatigue," "dental problems," "irregular periods," "GERD," or "muscle cramps."

High-yield history elements to elicit:

SCOFF screening questionnaire (≥2 positives suggests eating disorder):

Screen for suicidality at every visit — completed suicide rate is elevated; self-harm common.

Screen for substance use (stimulants, diet pills, ipecac, thyroid hormone misuse, insulin omission in T1DM).

Menstrual history: oligomenorrhea common but amenorrhea suggests anorexia crossover.

Social/functional: relationship strain, financial impact (food costs, dental bills), academic/occupational disruption.

Physical Exam Findings and Hemodynamic Assessment

— Perimolysis: erosion of lingual/palatal enamel of upper teeth (acid pools posteriorly when emesis is induced supine)

— Dental caries, increased temperature sensitivity

— Gingivitis, palatal petechiae/trauma from finger or object insertion

— Halitosis, xerostomia

— Bilateral painless parotid hypertrophy ("chipmunk cheeks") — sialadenosis from chronic vomiting; elevated serum amylase (salivary isoenzyme)

— Submandibular gland enlargement less common

— Russell sign: callus/abrasion on dorsum of dominant hand's knuckles from teeth during induced vomiting — pathognomonic

— Lanugo is uncommon in BN (more anorexia)

— Petechiae on face/conjunctivae from Valsalva during vomiting

— Orthostatic hypotension and tachycardia from volume depletion

— Bradycardia is less typical than in anorexia

— Listen for arrhythmias — hypokalemia/hypomagnesemia can produce prolonged QT, U waves, PVCs

Board pearl: A young woman with bilateral painless parotid swelling, elevated amylase, and normal lipase is BN until proven otherwise — the amylase is salivary isoenzyme, not pancreatic. Don't chase pancreatitis.

Key distinction: Russell sign and perimolysis both require self-induced vomiting — patients who purge only via laxatives/diuretics/exercise will lack these findings, making diagnosis harder.

Most patients with BN appear physically well and normal weight — exam findings are subtle and require targeted inspection.

Oral/dental (from recurrent vomiting):

Salivary glands:

Skin/extremities:

GI: epigastric tenderness, signs of GERD, occasionally rectal prolapse (laxative abuse)

Cardiopulmonary/hemodynamic:

Neuromuscular: proximal weakness, cramps (electrolyte disturbance); ipecac toxicity → cardiomyopathy with heart failure signs

Vitals red flags requiring admission: HR <40 or >110, SBP <90, orthostatic ΔHR >35, hypothermia <36°C, severe dehydration.

Diagnostic Workup — Initial Labs, ECG, and Biomarkers

— BMP/CMP: hypokalemia (most common), hypochloremia, hyponatremia, metabolic alkalosis (vomiting) or non-anion-gap metabolic acidosis (laxative-induced bicarbonate loss)

— Magnesium, phosphorus, calcium — often low; correct before/with potassium

— BUN/creatinine — elevated from volume depletion; chronic laxative use → prerenal azotemia

— Glucose — hypoglycemia in severe restriction

— CBC — mild anemia, leukopenia possible

— LFTs — mild transaminitis from fatty infiltration or refeeding

— Amylase — elevated (salivary fraction); lipase normal distinguishes from pancreatitis

— TSH — rule out hyperthyroidism mimic

— Urine pregnancy test in women of reproductive age

— Urinalysis — specific gravity for hydration; urine pH; urine chloride (<20 in vomiting, >20 in diuretic abuse — like the classic metabolic alkalosis workup)

— Look for QTc prolongation (risk of torsades)

— U waves (hypokalemia), flattened T waves, ST depression

— Bradycardia, low voltage if comorbid anorexia

Step 3 management: Always order ECG and electrolytes (including Mg and Phos) at the initial visit and at every follow-up while active purging continues. Hypokalemia + prolonged QT is the proximate cause of sudden death in BN.

Board pearl: Urine chloride <20 mEq/L → vomiting/remote diuretic; >20 → active diuretic abuse or Bartter/Gitelman.

BN is a clinical diagnosis (DSM-5 criteria) — labs are for assessing medical complications and ruling out mimics, not for confirming diagnosis.

Core initial labs (every new BN patient):

ECG — mandatory:

Bone density (DEXA) if menstrual irregularity ≥6 months or anorexia crossover history.

Stool studies if laxative abuse suspected — phenolphthalein/bisacodyl screen (rarely available, mostly historical).

Pseudo-Bartter syndrome: chronic vomiting/diuretic use → secondary hyperaldosteronism → resembles Bartter syndrome on labs (hypokalemia, alkalosis, elevated renin/aldo) — resolves with cessation but rebound edema during recovery is common and distressing.

Diagnostic Workup — Advanced and Confirmatory Studies

— Eating Disorder Examination (EDE) — gold standard interview

— EDE-Q (self-report version)

— Eating Attitudes Test (EAT-26) — screening

— Beck Depression Inventory, GAD-7, PHQ-9 for comorbidity

— Hematemesis (rule out Mallory-Weiss tear or Boerhaave)

— Persistent dysphagia, odynophagia

— Refractory GERD symptoms — assess for erosive esophagitis, Barrett's in chronic cases

— CXR or CT chest if Boerhaave (pneumomediastinum, left pleural effusion)

— Abdominal imaging if obstruction, ileus from laxative abuse, or superior mesenteric artery (SMA) syndrome in weight-restored patients

— Brain MRI only if atypical features (focal neuro signs, late onset, cognitive decline) — rule out hypothalamic tumor

— If ipecac abuse suspected — emetine cardiomyopathy (irreversible, dose-dependent)

— If symptoms of heart failure, syncope, or significant electrolyte derangement

Key distinction: Cyclic vomiting syndrome, gastroparesis, achalasia, and GERD can mimic BN's vomiting pattern but lack the cognitive criterion (body-image overvaluation) and the volitional, post-binge nature of emesis. A careful history — "Do you make yourself vomit?" asked nonjudgmentally — usually settles it.

Board pearl: Ipecac use → measure CK and obtain echo; emetine has a long half-life and cumulative cardiotoxicity that can progress even after cessation. Always ask specifically about ipecac in chronic BN.

BN diagnosis is made by structured psychiatric interview applying DSM-5 criteria — no imaging or biomarker confirms it. Advanced studies are for complications, comorbidities, and exclusion of organic mimics.

Structured/semi-structured instruments (used in specialty care):

Endoscopy (EGD): consider for

Imaging:

Echocardiogram:

DEXA scan: baseline if BN coexists with low BMI history, amenorrhea, or known osteopenia risk.

Endocrine workup for crossover or atypical cases: LH/FSH, estradiol, cortisol, IGF-1.

Hemoccult/colonoscopy rare — consider in chronic laxative abuse with melanosis coli, cathartic colon, or unexplained GI bleeding.

Risk Stratification and First-Line Management Logic

— Medically stable, no suicidality, able to engage in psychotherapy, supportive environment

— Initiate CBT-Enhanced (CBT-E) — first-line evidence-based psychotherapy for BN, typically 20 sessions over 20 weeks

— Add SSRI (fluoxetine) for moderate-severe symptoms or comorbid mood/anxiety

— Nutritional rehabilitation with registered dietitian: regular meal pattern (3 meals + 2–3 snacks), reduce dietary restriction (which drives binges)

— Dental referral

— PCP for medical monitoring (electrolytes, ECG)

— Failed outpatient, significant comorbidity, daily purging, inability to interrupt binge-purge cycle

— Suicidality, severe comorbid psychiatric illness, inability to control behaviors despite intensive outpatient

— K <3.0, Na <125 or >150, severe dehydration, syncope, QTc >500 ms, hematemesis, intractable vomiting, pregnancy with active purging, suicide risk with active behaviors

— CBT-E (psychotherapy gold standard)

— Fluoxetine 60 mg/day (only FDA-approved drug for BN)

— Family-based treatment (FBT) for adolescents

— Interpersonal psychotherapy (IPT) if CBT unavailable/declined (slower onset, similar long-term)

— Dialectical behavior therapy (DBT) if borderline traits or self-harm

Step 3 management: A stable adult outpatient with BN should receive CBT-E + fluoxetine 60 mg/day as combined first-line. Do NOT use bupropion (lowers seizure threshold — contraindicated in eating disorders).

Board pearl: Fluoxetine 60 mg (higher than the typical 20 mg antidepressant dose) is the specifically-studied effective dose for BN — answer choices often test this exact number.

Management decision tree hinges on (1) medical stability, (2) psychiatric acuity, (3) comorbidity burden, (4) treatment history.

Outpatient (most patients):

Intensive outpatient/partial hospitalization (PHP):

Inpatient psychiatric admission:

Inpatient medical admission criteria:

Treatment hierarchy (first-line → adjunct):

Pharmacotherapy — First-Line Drug Regimen

— Target dose: 60 mg/day (significantly higher than depression dosing)

— Start 20 mg, titrate over 1–2 weeks to minimize GI side effects

— Mechanism: reduces binge and purge frequency by ~50–75%; effect independent of antidepressant action

— Duration: continue ≥6–12 months after remission; relapse common if discontinued early

— Side effects: GI upset, insomnia, sexual dysfunction, decreased appetite (may be beneficial), QT prolongation (monitor with concurrent electrolyte issues)

— Bupropion: black-box contraindication in active eating disorders — increased seizure risk from electrolyte disturbance

— Tricyclic antidepressants: dangerous in overdose, anticholinergic, QT effects

— Stimulants (e.g., lisdexamfetamine): approved for BED, not BN — risk of abuse for weight suppression

— Benzodiazepines: avoid for "anxiety around eating" — dependence risk; use sparingly

Step 3 management: When the vignette asks the next best medication for BN, the answer is fluoxetine 60 mg/day. If the patient has a seizure disorder or is already on bupropion for depression, switch to fluoxetine — never add fluoxetine while continuing bupropion in active BN.

Board pearl: Topiramate's dual benefit (decreased binges + weight loss) makes it the high-yield answer when a patient has BN with obesity or migraine; remember kidney stones and teratogenicity.

Fluoxetine is the only FDA-approved medication for BN.

Other SSRIs (sertraline, citalopram, escitalopram) — off-label, used if fluoxetine intolerable; citalopram capped at 20 mg if QTc concerns (and 40 mg generally).

Topiramate — second-line; reduces binge frequency and body weight; dose 100–250 mg/day; side effects (cognitive slowing, paresthesias, kidney stones, teratogenic — cleft palate, avoid in pregnancy or use contraception); useful when weight loss is also a treatment goal.

Contraindicated/avoid:

Adjuncts for comorbidities: treat depression, anxiety, OCD, PTSD per standard guidelines, preferring SSRIs.

Special caution: rapid electrolyte correction during refeeding; monitor for refeeding syndrome if severely malnourished.

Psychotherapy and Non-Pharmacologic Management Depth

— 20 sessions over 20 weeks (40 sessions if underweight)

— Four stages: (1) engagement + behavioral change (regular eating, self-monitoring), (2) review/identify obstacles, (3) address overvaluation of shape/weight, dietary restraint, mood intolerance, (4) maintenance/relapse prevention

— Effects emerge by week 4–6; if no reduction in binge/purge by mid-treatment, intensify or switch

— First-line for adolescents with BN

— Three phases: parental control of eating → gradual return of autonomy → adolescent identity work

— Outperforms individual therapy in <18 population

— Comparable long-term efficacy to CBT but slower (focus on interpersonal triggers of binges)

— Reasonable if CBT unavailable or declined

— For BN with comorbid borderline personality, self-harm, severe emotion dysregulation

— Skills: mindfulness, distress tolerance, emotion regulation, interpersonal effectiveness

— Establish regular eating pattern (every 3–4 hours)

— Reintroduce "forbidden foods" gradually to reduce restriction-driven binges

— NOT calorie counting–focused; emphasize structure over restriction

CCS pearl: For an adolescent BN case on CCS, order: outpatient CBT-E or FBT, registered dietitian consult, dental referral, fluoxetine if ≥18 or moderate-severe symptoms, baseline labs/ECG, follow-up in 1–2 weeks, and advance the simulated clock to assess response.

Key distinction: CBT-E is first-line in adults; FBT is first-line in adolescents. Don't confuse them.

Cognitive Behavioral Therapy — Enhanced (CBT-E) — first-line, strongest evidence:

Family-Based Treatment (FBT / Maudsley approach):

Interpersonal Psychotherapy (IPT):

Dialectical Behavior Therapy (DBT):

Guided self-help CBT: structured workbook + brief clinician contact; reasonable initial step in mild cases or when specialty CBT unavailable.

Nutritional rehabilitation (registered dietitian):

Dental care: rinse with water (NOT brush) immediately after vomiting to avoid enamel abrasion; fluoride rinses; routine cleanings.

Exercise: if compulsive, restructure rather than prohibit.

Special Populations — Elderly and Renal/Hepatic Impairment

— Higher burden of cumulative complications: osteoporosis, dental loss, chronic kidney disease from chronic volume depletion/laxative abuse, esophageal strictures, cardiomyopathy (ipecac)

— Polypharmacy concerns — review for QT-prolonging agents (azithromycin, ondansetron, methadone, antipsychotics) interacting with fluoxetine

— Start SSRIs at lower doses (e.g., fluoxetine 10–20 mg) and titrate slowly; still aim for therapeutic 60 mg if tolerated

— Fluoxetine: hepatically metabolized — no dose adjustment for renal impairment in mild-moderate CKD; use cautiously in severe disease

— Topiramate: renally excreted — reduce dose if CrCl <70; avoid or adjust significantly in ESRD

— Avoid NSAIDs (often used informally by patients for headache) given volume-depletion AKI risk

— Correct hypokalemia gently to avoid rebound hyperkalemia; monitor K, Mg, Phos closely

— Fluoxetine: reduce dose or extend interval in cirrhosis (long half-life, active metabolite norfluoxetine accumulates)

— Avoid alcohol — common comorbidity worsens hepatic and electrolyte status

— On cessation of purging, secondary hyperaldosteronism persists transiently → fluid retention, edema, weight gain (often distressing and triggers relapse)

— Manage with spironolactone (50–100 mg/day) for 2–4 weeks, sodium restriction, patient education that weight gain is fluid not fat

Step 3 management: Counsel patients about rebound edema before they stop purging — anticipating this side effect prevents the relapse trap of "I gained 5 lbs in a week so vomiting must be necessary."

Board pearl: Spironolactone is the answer for post-purging rebound edema because it blocks the active hyperaldosteronism.

BN onset in older adults is uncommon but exists — usually represents a chronic, longstanding disorder rather than new onset. New eating-disorder symptoms in the elderly should prompt evaluation for depression, dementia, GI malignancy, medication side effect, or late-onset eating disorder.

Older adults with chronic BN:

Renal impairment:

Hepatic impairment:

Pseudo-Bartter rebound edema:

Special Populations — Pregnancy, Pediatrics, and Other Subgroups

— BN often improves during pregnancy but relapses postpartum (up to 50%)

— Active BN in pregnancy increases risk of: miscarriage, preterm birth, low birth weight, SGA, hyperemesis, gestational HTN, postpartum depression

— Fluoxetine: generally continued in pregnancy if benefits outweigh risks; class C; small risk of neonatal adaptation syndrome and PPHN — discuss risk/benefit, don't abruptly stop

— Avoid topiramate — teratogenic (cleft lip/palate, risk highest in first trimester)

— Folate supplementation, prenatal vitamins (often deficient)

— Screen all pregnant women for eating disorders — many hide it

— Coordinate OB + psychiatry + nutrition; monitor weight trajectory closely

— Postpartum: aggressive relapse prevention, screen for postpartum depression (much higher rate)

— FBT first-line — parents take temporary control of eating

— SSRIs less well studied in <18; use fluoxetine if needed (only SSRI with FDA pediatric depression approval) with FDA black-box on suicidality monitoring

— Growth, pubertal staging, bone density monitoring

— Confidentiality vs. parental involvement: weight, vitals, and safety concerns generally trump confidentiality

— Disordered eating + menstrual dysfunction + low bone density

— Reduce training load; nutritional repletion; address pressure from coaches

— Insulin omission to induce glycosuria/weight loss

— Markedly elevated risk of DKA, retinopathy, neuropathy, early mortality

— A1c trend + recurrent DKA admissions = red flag; coordinate endocrine + psychiatry

Key distinction: FBT for adolescents; CBT-E for adults — and avoid topiramate in pregnancy; continue fluoxetine in pregnancy if needed.

Board pearl: Recurrent DKA in a young woman with T1DM and unexplained weight fluctuations = insulin omission/diabulimia until proven otherwise.

Pregnancy:

Pediatrics/adolescents:

Athletes ("female athlete triad" / RED-S):

T1DM ("diabulimia"):

LGBTQ+ patients, men, athletes, and minority populations are systematically under-screened — ask directly.

Complications and Adverse Outcomes

— Hypokalemia (most common, most dangerous) — arrhythmia, weakness, rhabdomyolysis

— Hypomagnesemia, hypophosphatemia, hypocalcemia

— Metabolic alkalosis (vomiting) or non-anion-gap acidosis (laxative-induced HCO3 loss)

— Hyponatremia — water loading (mask weight or before weigh-ins), SIADH-like picture

— QT prolongation, torsades, sudden cardiac death — leading cause of mortality

— Ipecac (emetine) cardiomyopathy — irreversible

— Bradycardia, hypotension (with anorexia overlap)

— Mallory-Weiss tears — hematemesis after forceful vomiting

— Boerhaave syndrome — full-thickness esophageal rupture (rare, surgical emergency, Hamman crunch, left pleural effusion, pneumomediastinum)

— Erosive esophagitis, Barrett's esophagus (long-term risk)

— Gastric dilation/rupture (binge episodes — surgical emergency)

— Acute pancreatitis (rare; binges with alcohol)

— Laxative abuse: cathartic colon, melanosis coli, electrolyte loss, dependence

— Constipation upon stopping laxatives (often triggers relapse)

— Suicide is a leading cause of death

— Overall standardized mortality ratio ~2× general population (lower than anorexia but still elevated)

— High rates of substance use disorders, self-harm

Step 3 management: Hematemesis in a BN patient — first thought Mallory-Weiss tear (usually self-limited); but if chest pain + dyspnea + crepitus → Boerhaave → emergent CT, surgical consult, broad-spectrum antibiotics, NPO.

Board pearl: Sudden death in BN ≈ hypokalemic torsades. Always check ECG and QTc when admitting.

Electrolyte and acid-base:

Cardiac:

GI:

Dental: perimolysis, caries, tooth loss, TMJ dysfunction

Endocrine/reproductive: menstrual irregularity, infertility, miscarriage; in T1DM, accelerated microvascular complications

Renal: prerenal azotemia, hypokalemic nephropathy, pseudo-Bartter syndrome, nephrolithiasis (topiramate)

Musculoskeletal: osteopenia (esp. with crossover restriction), stress fractures

Psychiatric/mortality:

When to Escalate Care — Admission and Consult Triggers

— K <3.0 mEq/L (or symptomatic at higher levels)

— Na <125 or >150

— Severe dehydration, syncope, orthostatic ΔHR >35

— HR <40 or >110 (sustained)

— SBP <90, or orthostatic SBP drop >20

— Hypothermia <36°C

— QTc >500 ms or any arrhythmia

— Hematemesis or suspected Boerhaave/gastric rupture

— Refeeding syndrome risk (severe malnutrition, BMI very low, prolonged restriction)

— Pregnancy with active purging or hyperemesis

— Acute pancreatitis, AKI, intractable vomiting

— Active suicidal ideation with plan/intent or recent attempt

— Inability to control behaviors despite intensive outpatient

— Severe comorbid psychiatric illness destabilizing function

— Failure of step-down levels (PHP, IOP, residential)

— Psychiatry/eating disorder specialist — diagnostic confirmation, treatment plan

— Nutrition/registered dietitian — required for all

— Dentistry — for all with self-induced vomiting

— Cardiology — if arrhythmia, ipecac exposure, persistent QTc prolongation, cardiomyopathy concern

— GI — for hematemesis, refractory GERD, suspected esophageal injury

— Endocrinology — T1DM with insulin omission; osteoporosis management

— OB/Gyn — pregnancy, fertility, contraception

— Social work — disposition, financial, housing, insurance

CCS pearl: On CCS, a BN patient with K=2.6 and QTc 520 ms gets: continuous telemetry, IV KCl (peripheral 10 mEq/hr; central 20 mEq/hr max), IV magnesium sulfate 2 g, oral KCl supplementation, NPO if active vomiting, psychiatry consult, repeat ECG and BMP q4–6h until stable, then transition to floor with psychiatry follow-up.

Step 3 management: Always replete magnesium and phosphorus when correcting potassium — hypomagnesemia causes refractory hypokalemia.

Medical admission criteria (any one):

Psychiatric admission criteria:

Specialty consults:

Levels of care continuum: outpatient → intensive outpatient (IOP) → partial hospitalization (PHP, day program) → residential → inpatient psychiatric → medical floor → ICU.

Key Differentials — Other Eating Disorders

— Binges + compensatory behavior identical to BN BUT patient is significantly underweight (BMI typically <18.5)

— Treatment is more intensive (weight restoration paramount); fluoxetine has no proven benefit until weight restored

— Higher mortality than BN

— Restriction without binges; severe distortion; amenorrhea common

— Distinguishing feature: no binge/purge cycle

— Recurrent binges (≥1/week × ≥3 months) without compensatory behaviors

— Patients typically overweight/obese

— Most common eating disorder in US

— Treatment: CBT-E first-line; lisdexamfetamine (Vyvanse) is FDA-approved for moderate-severe BED (NOT for BN); topiramate, SSRIs (especially sertraline, fluoxetine) effective

— Food avoidance without body-image concerns (sensory aversion, fear of choking/vomiting, lack of interest)

— Typically children/adolescents; weight loss and nutritional deficiency but no overvaluation of shape

Key distinction: The single most important differential question on Step 3 is BMI / weight status:

— Underweight + binge/purge → anorexia nervosa B/P subtype

— Normal weight + binge/purge → bulimia nervosa

— Overweight + binges, no purging → binge-eating disorder

Board pearl: Purging disorder (purging without binges) = OSFED, treated similarly to BN with CBT-E and SSRI.

Anorexia nervosa, binge-eating/purging subtype:

Anorexia nervosa, restricting subtype:

Binge-eating disorder (BED):

Avoidant/restrictive food intake disorder (ARFID):

Pica: ingestion of non-nutritive substances; iron deficiency common precipitant

Rumination disorder: effortless regurgitation and re-chewing, no compensatory intent, no body-image overvaluation

Night eating syndrome: excessive evening/nighttime caloric intake; often comorbid with depression; not in DSM-5 main eating disorder section

Other Specified Feeding or Eating Disorder (OSFED): subthreshold BN (frequency or duration not met), atypical anorexia (normal weight despite restriction), purging disorder (purging without binges)

Key Differentials — Non-Eating-Disorder Causes

— Cyclic vomiting syndrome — discrete stereotyped episodes with symptom-free intervals; often migraine-associated

— Cannabinoid hyperemesis syndrome — chronic cannabis use, relief with hot showers, recurrent vomiting; resolves with cessation

— Gastroparesis — diabetic or idiopathic; postprandial vomiting, early satiety, gastric emptying study delayed

— GERD/PUD — heartburn, no induced vomiting, no body-image preoccupation

— Achalasia — regurgitation of undigested food, dysphagia, bird-beak on esophagram

— Intestinal obstruction, SMA syndrome, malignancy — anatomical/structural

— Pancreatitis — elevated lipase (not just amylase)

— Hyperthyroidism — weight loss, increased appetite, tremor, tachycardia, elevated free T4, suppressed TSH

— DKA — vomiting + abdominal pain + hyperglycemia + ketosis + anion-gap acidosis

— Addisonian crisis — vomiting, hypotension, hyperkalemia (opposite electrolyte pattern), hyperpigmentation

— Hypercalcemia, uremia — vomiting with characteristic labs

— Increased ICP — morning vomiting, papilledema, headache, focal signs

— Vestibular disease — vertigo prominent

— Migraine — headache-associated

— Major depression with poor appetite — weight loss without binges or compensatory behaviors

— OCD with food-related rituals — distinguish by absence of body-image overvaluation

— Anxiety disorders with somatic vomiting

— Body dysmorphic disorder — focus on body part other than weight/shape; no eating behaviors

— Factitious disorder / malingering — induced vomiting for secondary gain

Key distinction: The psychological criterion — overvaluation of body shape/weight in self-evaluation — anchors BN diagnosis. Without it, even recurrent vomiting is not BN.

Board pearl: Young patient with intractable vomiting and hot-shower bathing behavior = cannabinoid hyperemesis, not BN.

GI causes of vomiting:

Endocrine/metabolic:

Neurologic:

Psychiatric:

Medication-induced vomiting: opioids, chemotherapy, GLP-1 agonists, SSRIs themselves.

Pregnancy — always rule out in women of reproductive age.

Secondary Prevention, Discharge Plan, and Long-Term Management

— Confirm medical stability: stable electrolytes off IV repletion, QTc <450, no orthostasis, tolerating PO

— Step-down level of care determined: PHP, IOP, or outpatient

— Active treatment team in place: psychiatrist or therapist (CBT-E or FBT), registered dietitian, PCP, dentist

— Medication reconciliation: continue/initiate fluoxetine 60 mg/day; oral electrolyte supplementation if needed (KCl, Mg oxide); avoid bupropion, stimulants, diuretics

— Spironolactone for rebound edema if recently stopped purging

— Safety plan if suicidal ideation; means restriction

— Schedule first follow-up within 1 week for high-risk patients

— Cessation of binge-purge cycle

— Normalization of eating pattern

— Address core cognitive distortions (overvaluation of shape/weight)

— Treat psychiatric comorbidities (depression, anxiety, PTSD, substance use)

— Restore physical health (dental, bone, cardiac, GI)

— Relapse prevention (~30–50% relapse rate over 5 years)

— Fluoxetine ≥6–12 months after remission, often longer; gradual taper if discontinued

— Treat comorbidities per their own duration guidelines

— Regular meal/snack structure

— Avoid restrictive diets (drive binges)

— Mindful, non-compulsive exercise

— Limit weighing frequency

— Identify and rehearse coping strategies for triggers

— Annual labs/ECG while symptoms active; less frequent in sustained remission

— Dental cleanings every 3–6 months

— DEXA every 1–2 years if history of low weight/amenorrhea

— Contraception counseling — many medications teratogenic; pregnancy planning

Step 3 management: Fluoxetine should be continued at 60 mg/day for at least 6–12 months after remission to prevent relapse — early discontinuation is a common misstep.

Board pearl: Address rebound constipation (after laxative cessation) with osmotic agents like polyethylene glycol, not stimulant laxatives, plus fiber and hydration.

Discharge planning after acute medical or psychiatric admission:

Long-term treatment goals:

Continuation pharmacotherapy:

Lifestyle/behavioral:

Health maintenance:

Follow-Up, Monitoring Parameters, and Counseling Cadence

— Initial weeks: weekly visits with therapist; biweekly with prescriber; PCP every 2–4 weeks for medical monitoring

— Stabilizing phase: spacing to every 2–4 weeks

— Maintenance: monthly, then every 3 months

— Sustained remission >1 year: every 6–12 months

— Binge frequency, purge frequency, restriction patterns (self-monitoring logs)

— Weight (consider blinded weights if patient distressed)

— Vitals including orthostatics

— Mood, suicidality (PHQ-9, C-SSRS)

— Comorbidity status (anxiety, substance use)

— Medication adherence and side effects

— Treatment engagement (homework, attendance)

— BMP + Mg + Phos every 1–2 weeks initially, then monthly

— ECG at baseline, after dose changes, and if symptomatic

— Annual: CBC, CMP, lipid panel, HbA1c, vitamin D, B12

— DEXA: baseline if indicated, then every 1–2 years

— Psychoeducation: cycle of restriction → binge → purge; rebound edema; dental hygiene (rinse, don't brush after vomiting); avoidance of bupropion/diuretics

— Family/partner involvement when appropriate (especially adolescents — FBT)

— Trigger identification and coping skill rehearsal

— Body image and weight stigma work

— Relapse warning sign identification — return to skipped meals, increased weighing, weight-focused thoughts, isolated eating

— ≥50% reduction in binge/purge frequency by 4–6 weeks of CBT-E

— Full remission (no binges/purges × 4+ weeks) is the goal

CCS pearl: On CCS, advance the simulated clock to 1 week, then 2 weeks, then 4 weeks; recheck BMP/Mg/Phos, ECG, weight, mood/suicidality, binge-purge diary; titrate fluoxetine to 60 mg; document dietitian and therapist visits.

Step 3 management: Weekly visits during acute phase, transitioning to monthly with sustained remission, with at least one year of active treatment before considering medication taper.

Outpatient follow-up frequency:

Parameters to monitor at each visit:

Laboratory monitoring while actively symptomatic:

Counseling content:

Outcome metrics for response:

Transition of care: when stepping down levels, ensure warm handoff, shared records, and overlap visits; don't allow gaps.

Ethical, Legal, and Patient Safety Considerations

— Most states permit adolescent confidentiality for mental health, but safety concerns (suicidality, severe medical instability) override confidentiality

— FBT requires parental involvement by design — discuss with adolescent the necessity

— Document conversations about limits of confidentiality at intake

— BN patients usually retain capacity (in contrast to severe anorexia where cognition is compromised)

— Severe medical instability or active suicidal intent may justify involuntary psychiatric hold under state-specific statutes (e.g., 5150 in CA; varies by state)

— Force-feeding rarely indicated in BN (unlike anorexia)

— Child or elder abuse if disordered eating reflects coercion or neglect

— Adolescents whose caregivers actively obstruct treatment

— Active BN poses fetal harm — discuss risks without coercion; document shared decision-making; avoid teratogens (topiramate)

— Postpartum: screen aggressively for relapse and PPD; safety-plan child welfare

— Avoid clinical complicity in performance-driven weight loss; document advice against unhealthy weight requirements; advocate with athletic programs

— Discharge from inpatient → outpatient: highest relapse risk in first 30 days

— College/school transitions, military, deployment: ensure continuity prescriptions and warm handoff

— Pediatric → adult care transition

— Never prescribe bupropion in active eating disorder (seizure black-box)

— Avoid diuretics, stimulants, weight-loss medications

— Limit dispensing quantities if overdose risk (esp. TCAs, acetaminophen)

— Screen for firearm access when suicidality present

— Counsel on dangers of ipecac and over-the-counter "diet aids"

— Many specialty programs are out-of-network; advocate for parity (Mental Health Parity Act)

— Document medical necessity for higher levels of care thoroughly

Step 3 management: When an adolescent with BN refuses parental involvement, explain the limits of confidentiality at the outset, involve parents for safety/medical issues, and pursue FBT — the evidence base favors family inclusion.

Board pearl: Bupropion is contraindicated in eating disorders — a frequent "wrong-answer" trap; choose fluoxetine instead.

Confidentiality vs. parental involvement (adolescents):

Decisional capacity and refusal of treatment:

Mandatory reporting:

Pregnancy:

Athletes/coaches:

Transitions of care — high-risk handoff points:

Patient safety pearls:

Health systems/insurance:

High-Yield Associations and Rapid-Fire Clinical Facts

Board pearl: "Normal-weight young woman + parotid swelling + hypokalemic metabolic alkalosis + elevated amylase" = bulimia nervosa — pattern recognition wins this question every time.

Key distinction: BN vs. anorexia B/P subtype = weight; BN vs. BED = presence of compensatory behaviors.

Russell sign = knuckle calluses from self-induced vomiting (pathognomonic)

Perimolysis = lingual/palatal enamel erosion of upper teeth

Parotid hypertrophy + elevated salivary amylase + normal lipase = chronic vomiting

Pseudo-Bartter syndrome = hypokalemia + metabolic alkalosis + elevated renin/aldo from chronic vomiting/diuretic use; treat rebound edema with spironolactone

Urine chloride <20 = vomiting/remote diuretic; >20 = active diuretic abuse

Mallory-Weiss tear = hematemesis post-vomiting, usually self-limited

Boerhaave = full-thickness esophageal rupture; Hamman crunch + left pleural effusion + pneumomediastinum

Ipecac (emetine) cardiomyopathy = irreversible, cumulative; check echo, CK

Fluoxetine 60 mg/day = only FDA-approved drug for BN

Topiramate second-line; helps with binges + weight; teratogenic (cleft palate), kidney stones

Bupropion contraindicated in active eating disorders

Lisdexamfetamine = FDA-approved for BED, not BN

CBT-E = first-line psychotherapy in adults; FBT = first-line in adolescents

SCOFF questionnaire ≥2 = screen positive

DSM-5 frequency: ≥1 binge + compensation per week × ≥3 months

BMI typically normal in BN (≥18.5); underweight + binge/purge = anorexia B/P subtype

T1DM "diabulimia" = insulin omission → recurrent DKA, accelerated complications

Sudden death mechanism: hypokalemic torsades, QTc >500

Comorbidities: depression 70%, anxiety, PTSD, substance use, borderline traits

Most common purging method: self-induced vomiting (80–90%)

Rebound edema upon purging cessation → spironolactone

Laxative cessation → osmotic laxatives (PEG) + fiber, not stimulants

Dental hygiene post-emesis: rinse with water/fluoride, don't brush immediately

Pregnancy: continue fluoxetine if needed; stop topiramate

Long-term mortality SMR ~2× general population; suicide is leading non-medical cause

Adolescent BN: ensure FBT, parental involvement, fluoxetine if needed

Board Question Stem Patterns

Step 3 management: When stem describes "bilateral painless parotid swelling" in a young woman, the diagnosis is bulimia nervosa until something else is proven — fluoxetine 60 mg + CBT-E is the answer.

Board pearl: Memorize the fluoxetine 60 mg/day dose — it's a near-guaranteed distractor trap for "20 mg."

Pattern 1 — Classic recognition: A 22-year-old woman, BMI 23, presents with dental erosions, painless bilateral parotid swelling, and hypokalemia. → Next best step: SCOFF screening / diagnose BN / start fluoxetine 60 mg + CBT-E.

Pattern 2 — Drug to avoid: BN patient with comorbid depression and smoking cessation desire — which medication is contraindicated? → Bupropion (seizure risk).

Pattern 3 — Right dose: BN, started on fluoxetine 20 mg with partial response — next step? → Titrate fluoxetine to 60 mg/day.

Pattern 4 — Acid-base puzzle: Hypokalemic metabolic alkalosis + urine Cl <20 in a young woman with parotid swelling. → Self-induced vomiting (BN).

Pattern 5 — Adolescent management: 16-year-old with binge-purge behaviors, normal weight → first-line treatment? → Family-based treatment (FBT).

Pattern 6 — Rebound edema: BN patient stops vomiting, develops 5-lb weight gain and lower extremity edema in 1 week → diagnosis / treatment? → Pseudo-Bartter rebound edema; spironolactone.

Pattern 7 — Hematemesis post-binge: Post-vomiting small-volume hematemesis → Mallory-Weiss tear; large-volume + chest pain + crepitus → Boerhaave syndrome (emergent surgery).

Pattern 8 — BED vs BN: Patient with binges WITHOUT compensatory behaviors, BMI 32 → binge-eating disorder; first-line med = lisdexamfetamine (not for BN).

Pattern 9 — Diabulimia: T1DM young woman with recurrent DKA, normal weight, omitting insulin → diagnose diabulimia (BN with insulin omission as purging).

Pattern 10 — Admission triage: BN with K 2.4, QTc 530 → admit, continuous telemetry, IV K and Mg, psychiatry consult.

Pattern 11 — Pregnancy: BN patient pregnant on topiramate → discontinue topiramate (teratogen); continue/initiate fluoxetine if indicated.

Pattern 12 — Salivary amylase: Elevated amylase, normal lipase, parotid swelling → NOT pancreatitis; chronic vomiting (BN).

Pattern 13 — Treatment failure: Outpatient BN with persistent daily purging after 4 weeks of CBT and fluoxetine → escalate to PHP/IOP and consider topiramate add-on.

Pattern 14 — Confidentiality: Adolescent refuses parental involvement → safety overrides confidentiality, recommend FBT.

One-Line Recap

Bulimia nervosa is recurrent binge eating with compensatory behaviors (vomiting, laxatives, fasting, exercise) ≥1×/week × ≥3 months in a typically normal-weight patient with body-shape overvaluation, treated first-line with CBT-E plus fluoxetine 60 mg/day, with vigilant monitoring for hypokalemic torsades and aggressive avoidance of bupropion.

Board pearl: The exam-defining triad — normal BMI + parotid swelling + hypokalemic metabolic alkalosis — is bulimia nervosa; the management answer is CBT-E plus fluoxetine 60 mg daily.

Key distinction: Underweight + binges = anorexia B/P; normal weight + binges + compensatory = bulimia; overweight + binges, no compensation = binge-eating disorder — all share CBT-E but differ in medication and intensity of care.

Diagnose: SCOFF screen → DSM-5 criteria; key exam clues = perimolysis, Russell sign, painless parotid swelling, elevated salivary amylase with normal lipase; labs = hypokalemic metabolic alkalosis (urine Cl <20).

Stratify & admit when: K <3.0, QTc >500, syncope, hematemesis with suspected Boerhaave, refractory vomiting, severe suicidality, or pregnancy with active purging — replete K with Mg and Phos.

Treat: CBT-E (adults) or FBT (adolescents) + fluoxetine 60 mg/day (only FDA-approved drug); topiramate second-line; never bupropion, never stimulants in BN; lisdexamfetamine is for BED only; continue fluoxetine ≥6–12 months post-remission.

Prevent complications: dental rinse-don't-brush after emesis; spironolactone for rebound edema on purging cessation; PEG for constipation off laxatives; DEXA if low-weight history; screen pregnancy/T1DM ("diabulimia") populations aggressively; address comorbid depression, anxiety, PTSD, substance use, and ongoing suicide risk.