Pediatrics USMLE Practice Questions

A. Aortic valve regurgitation

This option implies aortic root dilation (e.g., Marfan, rheumatic disease), which causes a diastolic murmur and bounding pulses, BUT this patient’s findings center on malnutrition and purging, not connective tissue or valvular disease.

B. Recurrent infections

This option implies immune deficiency (e.g., neutropenia, HIV, asplenia). While severe malnutrition can impair immunity, the most classic and high-yield complication in this adolescent with hypothalamic amenorrhea is low bone density and fractures, not recurrent infections.

C. Ovarian cancer

This option implies a malignant ovarian neoplasm (often in older women, family history, or BRCA mutations). Amenorrhea from hypothalamic suppression and low BMI does not increase ovarian cancer risk; instead it lowers estrogen exposure.

D. Hyperphosphatemia

This option implies renal failure or massive cell lysis. In eating disorders, especially with vomiting and malnutrition, you more commonly see hypophosphatemia (especially in refeeding syndrome), not hyperphosphatemia.

E. Hyperkalemia

This option implies impaired renal excretion or tissue breakdown. Purging with vomiting or laxative/diuretic abuse more typically causes hypokalemia, BUT the stem specifically points to a purging-type eating disorder, making hyperkalemia unlikely.

G. Shortened QT interval

This option implies hypercalcemia. Eating disorders with malnutrition and vomiting more commonly cause electrolyte deficits (e.g., hypokalemia, hypomagnesemia) and prolonged QT, not shortened QT from hypercalcemia.

H. Hyperthyroidism

This option implies weight loss with tachycardia, heat intolerance, hyperreflexia. This patient is bradycardic and hypotensive with low BMI and amenorrhea from hypothalamic suppression, which are seen in starvation/anorexia, not hyperthyroidism.

A. Myocardial ischemia

This option implies coronary artery disease causing angina/MI, which occurs in older patients with atherosclerotic risk factors, BUT this is a 2-year-old with congenital shunt physiology, not coronary disease.

B. Thrombocytosis

This option implies reactive or myeloproliferative platelet increase, which can follow inflammation or iron deficiency, BUT chronic left-to-right shunt and pulmonary congestion classically lead to clubbing and pulmonary hypertension, not isolated thrombocytosis as the key complication.

C. Secondary hypertension

This option suggests renal disease or endocrine causes of high systemic blood pressure, BUT the main hemodynamic issue here is increased pulmonary blood flow and possible pulmonary hypertension, not systemic secondary hypertension as the primary expected complication.

D. Aortic dissection

This option implies connective tissue disease or severe uncontrolled hypertension in adults, BUT aortic dissection is extremely rare in a 2-year-old and is not a recognized complication of isolated VSD with pulmonary overcirculation.

F. Chronic kidney disease

This option implies chronic glomerular or systemic disease (e.g., diabetes, reflux nephropathy), BUT there are no renal findings (edema, hematuria, abnormal creatinine) and VSD with lung disease primarily causes pulmonary and cardiac complications like clubbing, not primary CKD.

B. Recommend increased dietary fiber and fluids

This option implies mild constipation managed with lifestyle changes, which helps prevention, BUT the child already has significant fecal impaction requiring pharmacologic disimpaction first (polyethylene glycol).

C. Administer a normal saline bolus

This option implies dehydration or shock, which would cause poor perfusion, tachycardia with hypotension, dry mucous membranes; BUT this child is hemodynamically stable with a clear mechanical problem—fecal impaction.

D. Obtain an abdominal contrast enema

This option implies concern for Hirschsprung disease or obstruction, which would present with delayed meconium, chronic severe constipation from infancy, or bilious vomiting; BUT this child has a typical history of functional constipation with stool withholding and normal exam aside from stool burden.

E. Start empirical broad-spectrum antibiotics

This option implies infection or sepsis (fever, toxicity, peritoneal signs), BUT he is afebrile, nontoxic, and his symptoms are mechanical from constipation, not infectious.

F. Proceed with emergent exploratory laparotomy

This option implies an acute surgical abdomen (peritonitis, severe tenderness, guarding, rebound, absent bowel sounds), BUT his abdomen is only mildly distended with active bowel sounds and no guarding or rebound, and a clear cause—hard stool—is identified.

A. Coxsackie meningitis

This option implies viral meningitis with headache, photophobia, and meningeal signs, BUT this child has focal asymmetric motor weakness and decreased reflexes, not meningeal symptoms.

C. HSV encephalitis

This option implies encephalitis with altered mental status, seizures, focal cortical signs, and temporal lobe involvement, BUT this patient is alert with isolated spinal motor deficits and no mental status changes.

D. Botulism

This option implies toxin-mediated neuromuscular blockade causing descending symmetric paralysis, cranial nerve palsies, and autonomic signs, BUT this patient has asymmetric lower extremity weakness post-viral illness, not descending paralysis or bulbar findings.

E. Tetanus

This option implies spastic paralysis with muscle rigidity, trismus (lockjaw), and painful spasms due to inhibitory interneuron blockade, BUT this patient has flaccid paralysis with decreased reflexes, not rigidity or spasms.

F. Guillain-Barre syndrome

This option implies acute inflammatory demyelinating polyneuropathy with symmetric ascending weakness and areflexia plus albuminocytologic dissociation in CSF (high protein, few cells), BUT this patient has asymmetric weakness and a cellular (lymphocytic) CSF with near-normal protein.

A. Pulmonary stenosis

This option implies congenital heart disease such as that seen in Noonan syndrome, which can resemble Turner but typically has pulmonic stenosis, NOT the Turner stigmata in this patient.

C. Severe acne

This option implies androgen excess (e.g., PCOS, congenital adrenal hyperplasia), which would cause hirsutism and heavy menses, BUT this patient has ovarian failure signs, not hyperandrogenism.

D. Hyperphagia

This suggests Prader-Willi syndrome (hyperphagia, obesity, hypotonia), BUT our patient has specific Turner stigmata and hypertension, not obesity or developmental delay features.

E. Ectopia lentis

This implies Marfan syndrome or homocystinuria, which present with tall stature, lens dislocation, and connective tissue features, BUT this girl is short with Turner-specific physical findings.

F. Alzheimer disease

This is classically associated with ApoE4, Down syndrome (trisomy 21), and advanced age; Turner syndrome mainly predisposes to cardiovascular and bone complications, not early Alzheimer disease.