Common misconceptions

Common mistake
Wrong: Purging causes hyperchloremic metabolic acidosis.
Right: Purging (vomiting) causes hypochloremic, hypokalemic metabolic alkalosis due to loss of HCl and secondary hyperaldosteronism from volume depletion.
Vomiting doesn't cause acidosis — it causes metabolic alkalosis because what's lost is hydrochloric acid (HCl) from the stomach. Losing H+ and Cl- raises serum bicarbonate and drops chloride. Volume depletion from purging then activates the renin-angiotensin-aldosterone system, which drives aldosterone to retain sodium at the cost of secreting more potassium and hydrogen into urine, deepening both the hypokalemia and the alkalosis. The full picture is hypochloremic, hypokalemic metabolic alkalosis — remember it as the opposite of what your gut tells you.
Common mistake
Wrong: Bupropion is a reasonable antidepressant choice in bulimia nervosa because it promotes weight loss.
Right: Bupropion is contraindicated in bulimia nervosa because it significantly lowers the seizure threshold, and electrolyte disturbances from purging further increase seizure risk.
Bupropion lowers seizure threshold as a class effect, and this risk is dramatically amplified in bulimia nervosa because purging causes hypokalemia and other electrolyte disturbances that independently destabilize neuronal membranes. The combination is dangerous enough that bupropion is explicitly contraindicated in any patient with an eating disorder involving purging. The fact that it promotes weight loss makes it seem appealing in this population — that's exactly why this misconception is so persistent, and exactly why the exam tests it.
Common mistake
Wrong: The standard antidepressant dose of fluoxetine (20 mg/day) is used for bulimia nervosa.
Right: Fluoxetine for bulimia nervosa requires a higher dose of 60 mg/day, which is FDA-approved specifically for this indication.
The standard antidepressant dose of fluoxetine is 20 mg/day for depression, but the FDA-approved dose for bulimia nervosa is 60 mg/day — three times higher. This higher dose was established in clinical trials and is specific to this indication. On USMLE Step 1, if a question asks about pharmacologic treatment of bulimia and your answer involves fluoxetine, the dose matters: 60 mg is the correct answer, and selecting 20 mg reflects treating bulimia like depression rather than recognizing it as a distinct indication with its own dosing.
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What the exam tests

  1. Know the diagnostic criteria: binges plus compensatory behaviors occurring at least once weekly for 3 months, with body image disturbance — and understand how this differs from anorexia nervosa (weight status, restriction vs. binge-purge).
  2. Identify the physical exam findings and lab pattern from chronic purging: parotid hypertrophy, dental enamel erosion, Russell sign, and the metabolic consequence — hypochloremic hypokalemic metabolic alkalosis, not acidosis.
  3. Select first-line management: CBT is the preferred psychotherapy, fluoxetine 60 mg/day is the FDA-approved pharmacologic agent, and bupropion is explicitly contraindicated due to seizure risk compounded by electrolyte disturbances.

Can you avoid these mistakes?

A 19-year-old woman presents with swollen cheeks, erosion of dental enamel, and calluses on the dorsal surface of her right hand. Labs show bicarbonate of 32, chloride of 92, and potassium of 3.0. What is the diagnosis, what is the acid-base disturbance, and what caused each electrolyte abnormality?
You are considering pharmacotherapy for a college student with bulimia nervosa who also reports depressed mood. She asks if she can take bupropion because she heard it helps with weight. How do you respond, and what do you prescribe instead at what dose?
A patient meets criteria for bulimia nervosa. She tells you her episodes happen about once every 2 weeks and have been going on for 6 weeks. Does she meet DSM criteria? What is the required frequency and duration?
Compare the expected electrolyte and acid-base findings in a patient with bulimia who purges by vomiting versus one who abuses laxatives. How does the mechanism differ, and what does that mean for the lab pattern in each case?

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