Match each clinical presentation of a patient with an eating or somatic symptom-related disorder to the most characteristic laboratory abnormality or physical finding associated with their condition.
- A college student of normal weight who reports cycles of consuming massive amounts of food followed by intentional emesis.Metabolic alkalosis featuring low serum chloride and low serum potassium, often accompanied by enlarged parotid glands.
- An aspiring dancer who frequently consumes over-the-counter senna and bisacodyl to control her shape, presenting with chronic watery stool.Non-anion gap metabolic acidosis featuring low serum potassium and proportionally elevated serum chloride.
- An adolescent track athlete presenting with severe dietary restriction, a body mass index of 14.2 kg/m², and fine downy body hair.Hypothalamic amenorrhea, low resting heart rate, and decreased systolic and diastolic blood pressure.
- A laboratory technician with recurrent symptomatic hypoglycemic episodes who secretly self-administers medication to gain medical attention without external reward.High circulating insulin concentration with concurrently suppressed endogenous C-peptide.
- A profoundly malnourished patient who develops acute heart failure and arrhythmias 48 hours after starting aggressive oral and intravenous nutritional supplementation.Profound depletion of serum phosphate, magnesium, and potassium driven by sudden cellular uptake.
Answer
Each clinical presentation aligns with a specific pathophysiological consequence: vomiting causes metabolic alkalosis; laxative abuse causes normal anion gap metabolic acidosis; starvation induces hypothalamic amenorrhea and bradycardia; exogenous insulin use suppresses C-peptide; and rapid refeeding shifts electrolytes intracellularly.
Each disorder leads to specific, identifiable clinical and laboratory findings based on its unique mechanism. Self-induced vomiting causes acid loss (alkalosis), while laxative abuse causes bicarbonate loss (acidosis). Severe starvation leads to hormonal suppression and bradycardia. Factitious hypoglycemia from exogenous insulin is proven by suppressed C-peptide, and refeeding syndrome is driven by insulin-mediated intracellular shifts of essential electrolytes.
Step-by-Step Solution
Key Concept
Differentiation of eating disorders and somatic symptom-related conditions through their distinct physiological, laboratory, and metabolic consequences.