USMLE Step 2 CK pediatrics questions

Breast milk jaundice is an unconjugated hyperbilirubinemia that develops after the first week of life in a well-appearing, adequately feeding, and appropriately growing breastfed infant. It is thought to result from substances in breast milk, such as beta-glucuronidase, that increase enterohepatic recirculation of bilirubin. This differs from breastfeeding failure jaundice, which occurs in the first days of life due to insufficient milk intake and is accompanied by weight loss and dehydration. The infant's good weight gain, effective feeding, and predominantly unconjugated bilirubin support breast milk jaundice.

• A. Biliary atresia presents with conjugated hyperbilirubinemia and acholic stools, not an isolated unconjugated elevation.
• B. Hemolytic disease typically presents in the first 24-48 hours of life, not at day 12 with a reassuring initial bilirubin trend.
• D. Breastfeeding failure jaundice occurs in the first days of life and is associated with poor feeding and weight loss, not present here.
• E. Sepsis-associated cholestasis would present with a rise in direct bilirubin and signs of systemic illness.

The AAP hour-specific bilirubin nomogram stratifies risk based on the infant's age in hours and total serum bilirubin level, guiding decisions on phototherapy. A total bilirubin of 15 mg/dL at 48 hours in a term infant without hemolysis falls in a range that crosses the phototherapy threshold, warranting initiation of phototherapy to prevent progression to severe hyperbilirubinemia and kernicterus. Phototherapy converts bilirubin into water-soluble photoisomers that can be excreted without conjugation. Exchange transfusion is reserved for markedly higher levels or when phototherapy fails.

• A. Simply repeating the level without intervention delays treatment when the threshold for phototherapy has already been met.
• B. Discontinuing breastfeeding is not recommended as first-line management of hyperbilirubinemia in a well infant.
• D. IVIG is reserved for hemolytic disease due to isoimmunization, not indicated given a negative direct antiglobulin test.
• E. Exchange transfusion is reserved for bilirubin levels that are markedly elevated or refractory to phototherapy, not met here.

The direct antiglobulin (Coombs) test detects antibodies bound to the surface of the infant's red blood cells and is the key confirmatory test for ABO or Rh hemolytic disease of the newborn. In this case, a type O mother and type A infant raise suspicion for ABO incompatibility, in which maternal anti-A or anti-B IgG antibodies cross the placenta and coat fetal red cells, leading to hemolysis and early jaundice. A positive direct Coombs test confirms antibody-mediated hemolysis. While a peripheral smear may show spherocytes and reticulocyte count may be elevated, these are supportive rather than confirmatory.

• A. A peripheral smear can show spherocytes suggestive of hemolysis but does not confirm the antibody-mediated mechanism.
• B. Haptoglobin is reduced in hemolysis but is nonspecific and not the confirmatory test.
• C. G6PD deficiency is a cause of hemolysis unrelated to the ABO/Rh setup described and would require a specific enzyme assay, not indicated as the first confirmatory step.
• E. Reticulocyte count reflects marrow response to hemolysis but does not confirm the immune mechanism.

An abnormal newborn screen for congenital hypothyroidism requires prompt confirmatory testing with serum free T4 and TSH, since the diagnosis must be confirmed and treatment started as early as possible, ideally within the first 2 weeks of life, to prevent irreversible intellectual disability. Many affected infants are asymptomatic at birth because transplacental maternal thyroid hormone provides temporary protection, so a normal physical examination does not rule out the disease. Treatment with levothyroxine should not be delayed for imaging studies, which can be obtained later to determine etiology without postponing therapy.

• B. Delaying confirmation and treatment risks irreversible neurodevelopmental damage; screening abnormalities must be addressed urgently.
• C. Maternal antibodies are relevant in specific scenarios like maternal autoimmune thyroid disease but are not a required or first step after an abnormal screen.
• D. Waiting for clinical signs to appear defeats the purpose of screening, as neurologic damage may already be occurring.
• E. Imaging can help determine the underlying cause but should not delay initiation of treatment once the diagnosis is confirmed.

Ampicillin plus gentamicin is the standard empiric regimen for early-onset neonatal sepsis because it covers the most common pathogens: group B Streptococcus, Escherichia coli, and Listeria monocytogenes. Ampicillin provides activity against GBS and Listeria, while gentamicin adds gram-negative coverage and acts synergistically with ampicillin against GBS. This combination is favored over broader-spectrum agents because it minimizes the development of resistance while covering the organisms responsible for the great majority of early-onset sepsis cases. Risk factors here include prolonged rupture of membranes (>18 hours), maternal intrapartum fever, and unknown GBS status, all of which raise suspicion for early-onset sepsis.

• A. Piperacillin-tazobactam alone lacks reliable activity against Listeria and is not standard empiric monotherapy for early-onset neonatal sepsis.
• C. Ceftriaxone should be avoided in neonates due to risk of biliary sludging and displacement of bilirubin from albumin; azithromycin does not cover the typical early-onset pathogens.
• D. Vancomycin and cefepime are reserved for late-onset or hospital-acquired sepsis with suspected resistant organisms, not first-line for early-onset disease.
• E. Clindamycin does not reliably cover gram-negative organisms like E. coli and is not part of standard empiric early-onset sepsis therapy.

Congenital CMV is the most common congenital infection in the United States and classically presents with sensorineural hearing loss, microcephaly, petechial rash ("blueberry muffin" lesions), and periventricular calcifications on neuroimaging. Occupational exposure to young children, such as working in a daycare, is a recognized risk factor for primary maternal CMV infection, which is frequently asymptomatic in the mother. In contrast, congenital toxoplasmosis classically causes diffuse intracranial calcifications, hydrocephalus, and chorioretinitis rather than periventricular calcifications and sensorineural hearing loss as the dominant finding. Diagnosis is confirmed by detecting CMV DNA via PCR in urine or saliva within the first 3 weeks of life.

• A. Congenital syphilis presents with findings such as snuffles, hepatosplenomegaly, and skeletal abnormalities (e.g., metaphyseal lucencies), not periventricular calcifications.
• C. Congenital rubella classically causes cataracts, sensorineural deafness, and patent ductus arteriosus ("triad"), not periventricular calcifications, and is now rare due to vaccination.
• D. Congenital Zika infection causes severe microcephaly with cortical malformations but is not associated with daycare exposure and is rare in the continental US.
• E. Toxoplasmosis typically causes diffuse (not periventricular) calcifications, hydrocephalus, and chorioretinitis, and is linked to exposure to cat feces or undercooked meat rather than daycare exposure.

Abdominal radiography, including supine and left lateral decubitus (or cross-table lateral) views, is the standard initial imaging study for suspected necrotizing enterocolitis (NEC) in a preterm infant. The left lateral decubitus view allows free intraperitoneal air (indicating perforation) to rise and be seen over the liver, while pneumatosis intestinalis (gas within the bowel wall) is the classic finding that confirms the diagnosis of NEC. Portal venous gas may also be seen in more severe cases. CT and contrast studies are not used in acute NEC because of radiation exposure, risk of perforation, and lack of added clinical benefit over plain radiographs in this unstable population.

• B. An upper GI contrast series is used to evaluate malrotation or obstruction, not NEC, and introducing contrast risks perforation in acute NEC.
• C. CT with contrast exposes a fragile preterm infant to unnecessary radiation and contrast risk and is not used for diagnosing NEC.
• D. Ultrasound can detect pneumatosis and portal venous gas in experienced hands but is not the standard confirmatory test; plain radiography remains first-line.
• E. Contrast enema is reserved for suspected distal obstruction (e.g., Hirschsprung disease) and is contraindicated in suspected NEC due to perforation risk.

Absence of any words by 18 months is a developmental red flag requiring prompt evaluation rather than watchful waiting. The first and most important step is to rule out hearing loss, since even mild or fluctuating conductive hearing loss from recurrent otitis media can significantly impair language acquisition, and this child's inconsistent response to her name combined with a history of recurrent otitis media raises specific concern for a hearing deficit. Audiologic evaluation is a quick, noninvasive, and essential first step before pursuing other diagnoses or interventions, since correcting a hearing problem may resolve the language delay. If hearing is normal, further developmental and autism screening would be the next step.

• A. Speech therapy may ultimately be appropriate but should follow, not precede, audiologic evaluation to identify a treatable underlying cause.
• B. No words by 18 months, combined with inconsistent response to name and a history of recurrent otitis media, is not reassuring and warrants evaluation.
• C. Brain MRI is not indicated as an initial test for isolated language delay without focal neurologic findings or regression.
• E. Delaying evaluation for 6 months is inappropriate given red-flag language delay at 18 months; prompt action, not watchful waiting, is recommended.

The American Academy of Pediatrics recommends universal autism spectrum disorder (ASD) screening with a standardized tool, such as the Modified Checklist for Autism in Toddlers, Revised with Follow-Up (M-CHAT-R/F), at both the 18-month and 24-month well-child visits, regardless of whether parents have expressed specific concerns. Universal screening is recommended because early signs of ASD may not be apparent to parents or may be subtle, and early identification allows for earlier intervention, which improves developmental outcomes. Referral to a developmental specialist is reserved for children who screen positive or who have clear clinical concerns on screening or examination, not applied universally regardless of findings.

• A. Direct referral for all children regardless of screening results is not standard practice and would overwhelm specialty services; referral should follow a positive or concerning screen.
• B. Fragile X testing is considered in specific clinical scenarios (e.g., intellectual disability with dysmorphic features or family history) and is not a routine universal screening tool for ASD at this visit.
• C. Screening based only on parental concern misses many children with ASD, since parents may not recognize early signs; universal screening at 18 and 24 months is recommended.
• D. Universal screening should occur at 18 months, not deferred until 24 months; both visits require screening.

This infant's growth pattern, with weight falling off more severely than length (a pattern typical of inadequate caloric intake), in the setting of a clear psychosocial stressor (formula dilution due to financial hardship) and an otherwise normal history and examination, is most consistent with nonorganic failure to thrive from inadequate caloric intake. Nonorganic failure to thrive is the most common cause of failure to thrive overall and should be strongly suspected when a feeding history reveals inadequate formula preparation or insufficient caloric provision, especially when the infant is otherwise well-appearing with no symptoms suggesting an organic disease. Organic causes are less likely here given the absence of GI symptoms, respiratory symptoms, or cardiac findings, and the clear alternative explanation. Management focuses on nutritional rehabilitation and addressing the underlying psychosocial and economic stressors, often with involvement of social work.

• A. Chronic urinary tract infection would typically present with fever, irritability, or other systemic signs, and is not suggested by this history.
• B. Cystic fibrosis typically presents with steatorrhea, recurrent respiratory infections, or meconium ileus, none of which are present in this infant.
• C. Celiac disease classically presents with diarrhea, abdominal distention, and poor growth after introduction of gluten, which is not described in this exclusively formula-fed infant.
• E. Congenital heart disease would typically present with poor feeding associated with tachypnea, diaphoresis with feeds, or a murmur, which are not described here.

MMR is a live attenuated vaccine. In immunocompromised hosts, particularly those with impaired cell-mediated immunity such as children on chemotherapy, the attenuated virus can replicate unchecked and cause severe or disseminated disease. Live vaccines (MMR, varicella, rotavirus, intranasal influenza, live attenuated zoster) are generally contraindicated during chemotherapy and should be deferred until adequate immune recovery, typically 3-6 months after completion of therapy. Inactivated vaccines remain safe and are still recommended during chemotherapy, though immune response may be blunted.

• B. MMR is a live vaccine, not an inactivated antigen preparation; this describes a different vaccine mechanism.
• C. MMR does not contain an adjuvant, and this is not the reason for deferral.
• D. This describes conjugate vaccines like Hib or pneumococcal vaccine, not MMR.
• E. MMR does not contain a recombinant protein, and there is no cross-reactivity with leukemic cells.

Capillary (fingerstick) lead tests are prone to environmental contamination and false positives, so any elevated capillary result must be confirmed with a venous blood lead level before further action. Once confirmed, management is guided by the venous level: levels of 3.5-44 micrograms/dL in an asymptomatic child are managed with environmental investigation and lead abatement rather than chelation, while levels of 45 micrograms/dL or higher typically warrant oral chelation, and levels of 70 micrograms/dL or higher with encephalopathy require inpatient IV chelation.

• A. A 6-month delay is inappropriate; the abnormal screening result requires prompt confirmatory testing.
• B. Chelation is not started before confirming the elevated result with a venous sample, and oral chelation is reserved for higher confirmed levels.
• D. An elevated capillary result cannot be dismissed without venous confirmation given the risk of false positives.
• E. IV EDTA is reserved for severe lead poisoning with encephalopathy, not an unconfirmed mildly elevated capillary level.

Whole cow's milk should not be introduced as the primary milk source before 12 months of age because it has low iron content and bioavailability, and its protein load can cause occult gastrointestinal blood loss in young infants, both of which increase the risk of iron deficiency anemia. Before 12 months, infants should receive breast milk or iron-fortified formula. After the first birthday, whole cow's milk is appropriate, and iron-rich complementary foods should be introduced around 6 months regardless of milk source.

• A. At 6 months, iron-fortified complementary foods are introduced, but cow's milk as the primary drink is still inappropriate.
• B. At 9 months, cow's milk still poses a risk of iron deficiency and gastrointestinal blood loss; it should be delayed until 12 months.
• C. At 4 months, infants should still be receiving breast milk or formula exclusively; cow's milk is far too early and risks anemia and renal solute overload.
• E. Delaying cow's milk until 18 months is unnecessarily late; it is considered safe starting at 12 months.

A femur fracture in a pre-mobile infant with no plausible accidental mechanism, combined with a posterior rib fracture (a location rarely caused by accidental trauma and strongly associated with squeezing or shaking), is highly concerning for physical abuse. The priority is to ensure the child's immediate safety by admitting for protection and evaluation while mandatorily reporting to child protective services for investigation. Osteogenesis imperfecta can mimic abuse but is excluded by history, examination, and normal bone density and should not delay protective reporting.

• A. A posterior rib fracture and femur fracture in a non-ambulatory infant are not consistent with common accidental injury.
• B. Bone densitometry may be considered later to evaluate for a rare bone fragility disorder but does not replace urgent safety measures and reporting.
• C. Genetic testing is not the immediate priority and should not delay protective intervention; it can be pursued if osteogenesis imperfecta remains a consideration.
• D. Discharging a pre-mobile infant with multiple suspicious fractures to an unsafe environment risks further harm and fails the obligation to protect the child.

Any infant younger than 28 days with a rectal temperature of 38.0°C (100.4°F) or higher is considered to have a fever of unclear source and is managed uniformly regardless of clinical appearance, because young neonates cannot reliably localize or display signs of serious bacterial infection and have immature immune defenses. Management requires hospital admission, a full sepsis evaluation including blood, urine, and cerebrospinal fluid cultures, and empiric broad-spectrum intravenous antibiotics (commonly ampicillin plus gentamicin or ampicillin plus cefotaxime) while awaiting results. This approach is universal in this age group because the risk of missing serious bacterial infection, including meningitis, is unacceptably high.

• A. Outpatient management without a full workup is unsafe in this age group because serious bacterial infection cannot be reliably excluded by clinical appearance alone.
• B. Oral antibiotics and outpatient management are inadequate; this age group requires IV antibiotics and inpatient admission pending full culture results.
• D. Brief emergency department observation is insufficient; neonates under 28 days require admission and a full diagnostic workup regardless of appearance.
• E. A single dose of ceftriaxone with outpatient discharge is used in some older, well-appearing, low-risk febrile infants, not in infants under 28 days.

Roseola infantum, caused by human herpesvirus 6, classically presents in infants and toddlers with several days of high fever that resolves abruptly, followed by the appearance of a maculopapular rash that begins on the trunk and spreads outward, often with the child appearing well despite the high fever. This rash-after-fever pattern distinguishes roseola from measles and rubella, in which the rash appears while fever is still present. The lack of cough, coryza, and conjunctivitis also argues against measles.

• A. Fifth disease (erythema infectiosum) causes a "slapped cheek" facial rash often with little or no preceding high fever, not a rash appearing after fever resolves.
• B. Scarlet fever presents with fever plus a sandpaper-textured rash and pharyngitis occurring together, not a rash that follows fever resolution.
• C. Rubella typically causes a milder fever with the rash appearing concurrently along with posterior auricular or occipital lymphadenopathy, not after fever resolution.
• E. Measles presents with fever accompanied by cough, coryza, and conjunctivitis, with the rash appearing while the fever is still high, not after defervescence.

This child's clinical picture (fever, cough, coryza, conjunctivitis, Koplik spots, and a cephalocaudal maculopapular rash) is classic for measles. Measles is a nationally notifiable disease in the United States, and any suspected case requires immediate airborne isolation and prompt reporting to the local or state health department to enable contact tracing and outbreak control. There is no specific antiviral treatment for measles; management is supportive, including vitamin A in appropriate cases. Failing to isolate and report risks further transmission, especially to unvaccinated or immunocompromised individuals.

• A. Acyclovir is used for herpesvirus infections, not measles, which has no specific antiviral therapy.
• B. Measles requires isolation and mandatory public health reporting; simple reassurance ignores the risk of transmission.
• C. Penicillin treats bacterial infections such as streptococcal pharyngitis, not a viral exanthem.
• E. A throat culture is not indicated because the clinical diagnosis of measles is already established by Koplik spots and the rash pattern.

Erythema infectiosum (fifth disease), caused by parvovirus B19, classically presents with a prodrome of low-grade fever and mild respiratory symptoms followed days later by the sudden appearance of bright red cheeks with circumoral pallor (the slapped-cheek sign), followed by a lacy, reticulated rash on the extremities and trunk. By the time the rash appears, the child is typically afebrile and no longer contagious. Diagnosis is clinical, and management is supportive, since the illness is self-limited in immunocompetent children.

• A. Kawasaki disease requires prolonged fever of 5 days or more plus mucocutaneous findings, which are absent in this well-appearing, afebrile child.
• B. Rubella presents with a cephalocaudal maculopapular rash and postauricular/suboccipital lymphadenopathy, not slapped cheeks.
• C. Measles features Koplik spots and a cephalocaudal rash with high fever, which is not described here.
• E. Scarlet fever presents with a sandpaper-textured rash and strawberry tongue, not a slapped-cheek appearance.

This presentation of painful oral ulcers combined with vesicular lesions on the palms, soles, and buttocks in a young child with a daycare exposure is classic for hand-foot-mouth disease, most commonly caused by coxsackievirus A16 (an enterovirus). The disease is typically self-limited and spreads via fecal-oral and respiratory droplet routes, making outbreaks common in daycare settings. Management is supportive with attention to hydration and pain control, since oral lesions can cause poor intake.

• A. Group A Streptococcus causes pharyngitis or scarlet fever, not vesicular lesions on the extremities.
• B. Varicella-zoster virus causes diffuse vesicular lesions in different stages across the trunk and face, not a palm/sole/mouth distribution.
• C. Herpes simplex virus typically causes gingivostomatitis confined to the mouth and perioral region, without the characteristic palm and sole distribution.
• D. Epstein-Barr virus causes mononucleosis with pharyngitis and lymphadenopathy, not vesicular skin lesions.

Scarlet fever is caused by group A Streptococcus strains that produce erythrogenic exotoxin, leading to pharyngitis, strawberry tongue, and a sandpaper rash with circumoral pallor. First-line treatment for confirmed group A streptococcal pharyngitis, including scarlet fever, in a patient without penicillin allergy is a 10-day course of oral penicillin V or amoxicillin, which is effective, narrow-spectrum, and prevents complications such as rheumatic fever and glomerulonephritis. Amoxicillin is often preferred in children due to better palatability as a suspension.

• A. Azithromycin is reserved for patients with penicillin allergy, not first-line therapy, and has rising resistance rates among group A Streptococcus.
• C. Intramuscular ceftriaxone is unnecessary when oral therapy is tolerated and not first-line for uncomplicated scarlet fever.
• D. Trimethoprim-sulfamethoxazole does not reliably eradicate group A Streptococcus and does not prevent rheumatic fever.
• E. Doxycycline is not recommended for streptococcal pharyngitis and is generally avoided in young children due to dental staining.

The most feared complication of Kawasaki disease is coronary artery aneurysm formation, which develops in up to 25% of untreated patients and in a smaller but still significant proportion even with timely IVIG treatment. Echocardiography is the standard imaging modality to assess coronary artery dimensions and should be performed at diagnosis, then repeated at approximately 1-2 weeks and 6-8 weeks after disease onset to monitor for aneurysm development. This surveillance guides decisions on antiplatelet or anticoagulant therapy duration and activity restrictions.

• A. Lumbar puncture has no role in screening for cardiac complications of Kawasaki disease.
• B. Abdominal ultrasound is not relevant to coronary artery surveillance in Kawasaki disease.
• C. An electrocardiogram alone can show nonspecific changes but cannot directly visualize or measure coronary artery dilation.
• D. A chest radiograph does not adequately visualize the coronary arteries and is not the screening tool of choice.

This infant has classic bronchiolitis, most commonly caused by RSV, presenting with upper respiratory symptoms followed by wheezing, crackles, and mild respiratory distress in a child under 2 years old. Management is supportive: nasal suctioning to relieve upper airway obstruction, ensuring adequate hydration and feeding, and close observation, since bronchiolitis is a self-limited viral illness. Bronchodilators, corticosteroids, and antibiotics have not been shown to improve outcomes in routine bronchiolitis and are not recommended by the American Academy of Pediatrics. Diagnosis is clinical; imaging is unnecessary unless there is concern for an alternative diagnosis or the patient is critically ill.

• B. Bronchiolitis is viral; antibiotics are not indicated unless a secondary bacterial infection is suspected.
• C. Bronchodilators do not improve outcomes in bronchiolitis and are not recommended for routine use.
• D. Chest radiography is not routinely indicated in typical bronchiolitis and does not change management.
• E. Corticosteroids have not been shown to be effective in bronchiolitis and are not part of standard management.

This child has croup (laryngotracheobronchitis), confirmed by the classic barky cough, inspiratory stridor, and the steeple sign on neck radiograph showing subglottic narrowing. Because he has stridor at rest with retractions, indicating moderate severity, nebulized racemic epinephrine should be added to dexamethasone to rapidly reduce airway edema via mucosal vasoconstriction, providing short-term relief while the steroid takes effect over several hours. Albuterol targets bronchospasm in the lower airways and has no role in croup, which is an upper airway process. Antibiotics are not indicated since croup is viral (most commonly parainfluenza virus).

• B. Heliox is not standard first-line therapy and is reserved for severe, refractory cases.
• C. Albuterol is a bronchodilator for lower airway bronchospasm and has no role in croup, an upper airway disease.
• D. Croup is viral; antibiotics are not indicated unless bacterial tracheitis or another superinfection is suspected.
• E. Intubation is reserved for impending respiratory failure, not indicated in this alert child tolerating oral intake with stable oxygen saturation.

This child's presentation, high fever, drooling, muffled voice, tripod positioning, and respiratory distress without cough, is classic for acute epiglottitis, historically caused by Haemophilus influenzae type b in unvaccinated children. Because the airway can obstruct completely and suddenly, the priority is securing the airway in a controlled environment, typically the operating room, with anesthesia and otolaryngology ready to perform emergent intubation or tracheostomy if needed. Any agitating maneuver, including throat examination with a tongue depressor, neck repositioning, or imaging that delays airway management, risks precipitating complete airway obstruction and should be avoided until the airway is secured.

• A. Radiographs delay definitive airway management and are unnecessary when the clinical picture is classic; distressing or repositioning the child risks acute obstruction.
• B. Direct oropharyngeal examination can trigger laryngospasm and complete airway obstruction in epiglottitis and should be avoided.
• C. While antibiotics are eventually needed, airway security takes priority over establishing IV access and giving antibiotics first in a child at risk of sudden obstruction.
• E. Epinephrine targets subglottic edema in croup, not supraglottic swelling in epiglottitis, and delays definitive airway management.

Bacterial tracheitis is a bacterial superinfection, most commonly with Staphylococcus aureus, that can follow a viral croup-like illness and presents with high fever, toxic appearance, and copious purulent secretions, with poor or absent response to racemic epinephrine, unlike classic viral croup. This clinical picture, especially the lack of response to epinephrine and systemic toxicity, should prompt suspicion for bacterial tracheitis, which requires airway management readiness, blood and airway cultures, and broad-spectrum antibiotics covering S. aureus (including MRSA) and respiratory flora. A barky cough and inspiratory stridor can occur in both conditions and are not distinguishing. Bacterial tracheitis typically occurs in the same age range as croup and often follows an initial viral prodrome, so age and recent croup diagnosis alone do not differentiate the two.

• A. Bacterial tracheitis commonly follows an initial viral illness resembling croup, so a recent croup diagnosis does not rule it out or distinguish it.
• C. Bacterial tracheitis occurs in a similar age range to croup, so age alone does not differentiate the two.
• D. A barky cough is common to both viral croup and bacterial tracheitis and does not distinguish between them.
• E. Inspiratory stridor at rest occurs in both conditions and is not a distinguishing feature.

An elevated immunoreactive trypsinogen (IRT) on newborn screening is suggestive but not diagnostic of cystic fibrosis, and the confirmatory test is the quantitative pilocarpine iontophoresis sweat chloride test. A sweat chloride concentration of 60 mEq/L or greater on two occasions confirms the diagnosis, while a value under 30 mEq/L makes it unlikely; intermediate values (30-59 mEq/L) warrant CFTR genetic testing. Genetic mutation panels are useful adjuncts, particularly for borderline sweat chloride results or for carrier screening, but they do not detect all CFTR mutations and are not the primary confirmatory test. Sweat chloride testing is reliable from about 2 weeks of age onward in a well-hydrated, adequately sized infant.

• A. CFTR genetic testing is a secondary or adjunctive test used when sweat chloride results are borderline, not the primary confirmatory test.
• C. Stool elastase assesses pancreatic exocrine function and is used to monitor pancreatic insufficiency, not to confirm the diagnosis.
• D. Nasal potential difference testing is a specialized research tool used in rare equivocal cases, not standard confirmatory testing.
• E. A chest radiograph does not diagnose cystic fibrosis and would be normal at this early asymptomatic stage.

The clinical picture of paroxysmal cough with inspiratory whoop and post-tussive vomiting in a young infant is classic for pertussis, and the preferred diagnostic test, especially within the first three weeks of cough, is PCR of a nasopharyngeal swab or aspirate, which offers high sensitivity and rapid turnaround. Culture on Bordet-Gengou medium is highly specific but slow and less sensitive, limiting its clinical utility despite being historically the gold standard. Serology is more useful later in the illness (after about 2 weeks) when PCR sensitivity declines, but it is not the preferred initial test. Marked lymphocytosis may support the diagnosis but is nonspecific and not confirmatory.

• A. Sputum culture for pertussis has low sensitivity and slow turnaround, making it impractical as the primary diagnostic test.
• B. Chest radiograph may show nonspecific findings or be normal and does not confirm pertussis.
• C. A CBC may show lymphocytosis supporting the diagnosis but is nonspecific and cannot confirm pertussis.
• E. Serologic antibody testing is more useful later in the illness and is not the preferred initial confirmatory test.

Projectile, non-bilious vomiting in an infant around 3-6 weeks of age, a palpable olive-shaped epigastric or right upper quadrant mass, and a hypochloremic, hypokalemic metabolic alkalosis are the classic triad of hypertrophic pyloric stenosis. The alkalosis results from loss of hydrochloric acid in vomitus combined with renal compensation that paradoxically excretes potassium and hydrogen while conserving sodium and causing a hypokalemic, hypochloremic metabolic alkalosis. Diagnosis is confirmed by abdominal ultrasound showing a thickened, elongated pylorus, and treatment is pyloromyotomy after fluid and electrolyte correction. Malrotation and duodenal atresia typically present with bilious vomiting, which is absent here.

• B. GERD causes non-forceful regurgitation without a palpable mass or significant electrolyte derangement.
• C. Congenital adrenal hyperplasia (salt-wasting type) causes hyponatremia and hyperkalemia, the opposite electrolyte pattern seen here.
• D. Duodenal atresia presents in the first days of life with bilious or non-bilious vomiting and a double-bubble sign on imaging, not at 5 weeks with an olive mass.
• E. Malrotation with volvulus presents with bilious vomiting and is a surgical emergency, not the pattern described here.

The combination of episodic colicky abdominal pain, lethargy between episodes, a sausage-shaped abdominal mass, and red mucoid (currant jelly) stool is classic for ileocolic intussusception, and the best initial test is abdominal ultrasound, which shows the characteristic target or doughnut sign on cross-section with high sensitivity and specificity. Ultrasound avoids radiation and can be performed quickly at the bedside, making it the preferred diagnostic modality in children. Once the diagnosis is confirmed and there are no signs of perforation or peritonitis, an air or contrast enema is both diagnostic and therapeutic, reducing the intussusception in most cases. Plain radiographs may show nonspecific findings and cannot reliably confirm the diagnosis.

• A. CT exposes the child to unnecessary radiation and is not needed when ultrasound can make the diagnosis.
• B. Plain abdominal radiographs are insensitive for intussusception and are used mainly to screen for free air or obstruction, not to confirm the diagnosis.
• D. MRI is not practical or necessary for this acute presentation and is not the standard diagnostic test.
• E. Contrast (or air) enema is the treatment of choice after ultrasound confirms the diagnosis, but it is not the first diagnostic test performed.

Bilious vomiting in a neonate with signs of hemodynamic instability, abdominal tenderness, and guarding suggests midgut volvulus complicating malrotation, a surgical emergency in which delay risks bowel ischemia and necrosis from twisting of the mesenteric vessels. When there are peritoneal signs or shock, the infant should proceed directly to emergency exploratory laparotomy (Ladd procedure) rather than first obtaining confirmatory imaging, because the risk of bowel necrosis outweighs the diagnostic benefit of further imaging. In a stable infant without peritonitis, an upper GI contrast series showing an abnormal duodenojejunal junction position (corkscrew sign) would be the test of choice, but this child's instability mandates immediate surgery. Delaying for additional imaging in an unstable child risks irreversible bowel loss.

• A. Nasogastric decompression alone is inadequate; this is a surgical emergency requiring prompt operative intervention.
• B. Ultrasound can show the whirlpool sign of volvulus but should not delay surgery in an infant with peritoneal signs and shock.
• D. An upper GI series is appropriate in a stable infant without peritonitis, but this unstable infant with guarding needs immediate surgery, not further imaging.
• E. Barium enema evaluates the colon and is not useful for diagnosing midgut volvulus, which involves the small bowel.

Failure to pass meconium within 48 hours of life, abdominal distention relieved by explosive stool release on rectal examination, and a contrast enema showing a transition zone between a narrow distal segment and dilated proximal colon are characteristic of Hirschsprung disease, caused by absence of ganglion cells in the distal bowel leading to functional obstruction. Definitive diagnosis requires rectal suction biopsy demonstrating absent ganglion cells and hypertrophied nerve trunks. Meconium ileus, typically associated with cystic fibrosis, presents with a microcolon on contrast enema rather than a discrete transition zone, and the explosive rectal exam response (squirt sign) is characteristic of Hirschsprung, not meconium ileus. Meconium plug syndrome usually resolves after the plug passes, often during the rectal exam or enema, without a persistent transition zone.

• A. Meconium ileus shows a microcolon with filling defects from inspissated meconium, not a discrete rectosigmoid transition zone, and is associated with cystic fibrosis.
• B. Meconium plug syndrome typically resolves after passage of the plug and does not show a persistent transition zone on enema.
• C. Anorectal malformation presents with an absent or abnormally positioned anal opening on inspection, not a normal-appearing anus with a radiographic transition zone.
• D. Congenital hypothyroidism can cause constipation but does not produce a transition zone on contrast enema and presents with other features like lethargy and macroglossia.

Direct (conjugated) hyperbilirubinemia in an infant with acholic stools and dark urine is concerning for biliary atresia, and prompt evaluation is critical because surgical outcomes with the Kasai hepatoportoenterostomy are significantly better when performed before 45-60 days of life. The initial workup includes abdominal ultrasound to assess for a gallbladder and biliary structures, followed by hepatobiliary scintigraphy or direct cholangiography (intraoperative cholangiogram) if biliary atresia remains suspected, since delay worsens irreversible liver fibrosis. Any direct bilirubin elevation in an infant, defined as greater than 1 mg/dL or more than 20% of total bilirubin, is never physiologic and warrants urgent evaluation. Phototherapy targets unconjugated hyperbilirubinemia and has no role here.

• A. Breast milk jaundice causes unconjugated, not conjugated, hyperbilirubinemia, and stopping breastfeeding would not address this infant's findings.
• C. Awaiting serology results delays time-sensitive evaluation; biliary atresia workup must proceed urgently given the narrow window for successful Kasai surgery.
• D. Phototherapy treats unconjugated hyperbilirubinemia; it is ineffective and inappropriate for conjugated hyperbilirubinemia.
• E. Physiologic jaundice is unconjugated and resolves by 2 weeks of age; direct hyperbilirubinemia with acholic stools is always pathologic and requires urgent evaluation.

This infant has the classic presentation of uncomplicated gastroesophageal reflux ("happy spitter"): frequent regurgitation with normal growth, good feeding, and a benign examination. Weight gain that tracks appropriately on the growth curve and the absence of projectile vomiting or a palpable olive-shaped mass argue strongly against pyloric stenosis. No imaging or medication is needed when growth is normal and the infant is thriving; management is reassurance, smaller/more frequent feeds, and upright positioning after feeds, with resolution expected by 12-18 months of age.

• A. Pyloromyotomy is treatment for confirmed pyloric stenosis, which is not suggested by this infant's presentation.
• B. An upper GI series is unnecessary when the clinical picture and growth are reassuring for simple reflux.
• D. PPIs are not recommended for uncomplicated reflux in a thriving infant without signs of esophagitis or feeding refusal.
• E. Ultrasound is reserved for suspected pyloric stenosis, which presents with projectile vomiting, weight loss, and a palpable olive-shaped mass, none present here.

This child's growth faltering with chronic diarrhea, bloating, and iron-deficiency-type anemia on a gluten-containing diet is classic for celiac disease. The recommended initial screening test is serum IgA anti-tissue transglutaminase (anti-tTG IgA) antibody, which has high sensitivity and specificity in children older than 2 years; a total serum IgA should be checked concurrently to exclude IgA deficiency, which can cause a false-negative result. A positive serology prompts endoscopic duodenal biopsy for confirmation. Treatment is a lifelong gluten-free diet.

• A. Stool culture evaluates for infectious diarrhea, which does not explain this chronic pattern of growth faltering.
• C. Sweat chloride testing is used to diagnose cystic fibrosis, which more commonly presents with respiratory symptoms and fatty stools, not the leading consideration here.
• D. Fecal elastase evaluates for pancreatic exocrine insufficiency (e.g., cystic fibrosis), not the most likely diagnosis here.
• E. Lactose intolerance typically causes isolated diarrhea and bloating without growth failure or anemia of this degree.

This child has the classic features of an innocent murmur, specifically Still's murmur: a soft, musical, vibratory, low-grade (grade 1-3/6) systolic murmur that is positional, becoming louder in the supine position and softer or disappearing with standing, with no associated symptoms, thrills, or diastolic component. Innocent murmurs occur in a structurally normal heart due to physiologic flow and require no further workup beyond reassurance when classic features and a normal exam are present. Pathologic murmurs are typically louder, harsh, holosystolic or diastolic, or associated with a thrill, cyanosis, or growth failure.

• A. Hypertrophic cardiomyopathy produces a harsh systolic murmur that increases with standing or Valsalva, the opposite of this murmur's behavior.
• B. An ASD murmur is a systolic ejection murmur at the upper left sternal border with a fixed split S2, not a vibratory lower sternal border murmur.
• D. Mitral regurgitation produces a holosystolic murmur radiating to the axilla, which is uncommon in an asymptomatic child with this described murmur.
• E. A VSD murmur is typically a harsh, holosystolic murmur at the left lower sternal border, often with a thrill, not a soft vibratory and positional murmur.

Small muscular VSDs have a high rate of spontaneous closure, often by 2 years of age, because muscular septal tissue grows and contracts around the defect during normal myocardial development. Infants with small defects, normal pulmonary pressures, and no heart failure or growth failure are managed expectantly with serial clinical and echocardiographic follow-up rather than early surgery. Surgical or catheter closure is reserved for defects causing significant left-to-right shunting, heart failure, failure to thrive, or pulmonary hypertension.

• B. Pulmonary vascular resistance is normal in this infant, and small defects with low shunt volume do not drive pulmonary hypertension.
• C. Small muscular VSDs typically shrink or close rather than enlarge; growth of the defect would be atypical.
• D. Eisenmenger syndrome results from longstanding large, uncorrected left-to-right shunts, not small restrictive defects with normal pulmonary pressures.
• E. VSDs do not change anatomic location or type over time; muscular and membranous defects are distinct anatomic entities.

This infant is having a hypercyanotic "tet spell," triggered by crying or agitation, which increases right-to-left shunting across the VSD and infundibular outflow obstruction. The immediate step is to calm the infant, place them in the knee-to-chest position (or squatting in older children) to increase systemic vascular resistance and reduce right-to-left shunting, and give supplemental oxygen. If this fails, subsequent measures include morphine, IV fluids, and phenylephrine; propranolol can be used for prevention of recurrent spells. The decrease in murmur intensity reflects reduced flow across the narrowed right ventricular outflow tract, a sign of worsening obstruction, not improvement.

• B. Digoxin is used for heart failure or rate control in certain arrhythmias and has no role in acute tet spell management.
• C. Balloon atrial septostomy is a procedure for transposition of the great arteries to improve mixing, not an immediate treatment for a tet spell.
• D. Diuretics are used for volume overload states like heart failure, not for acute hypercyanotic spells from dynamic right ventricular outflow obstruction.
• E. Dopamine is an inotrope used in shock states and is not first-line for tet spells; it does not address the dynamic outflow obstruction.

Coarctation of the aorta classically presents with hypertension in the upper extremities and lower blood pressure in the lower extremities, along with weak, delayed femoral pulses relative to brachial pulses (radiofemoral delay). The murmur is often heard posteriorly over the back due to turbulent flow at the coarctation site and collateral vessels, and rib notching on chest x-ray reflects erosion from dilated collateral intercostal arteries bypassing the obstruction. This combination of findings is diagnostic and should prompt echocardiography to confirm the diagnosis and plan repair.

• A. Takayasu arteritis can cause pulse and pressure discrepancies but is far less common in this age group and would not typically cause rib notching.
• C. Aortic stenosis causes a systolic ejection murmur radiating to the carotids, without a limb blood pressure differential or rib notching.
• D. PDA causes a continuous "machinery" murmur and does not typically cause a blood pressure gradient between upper and lower extremities.
• E. Renal artery stenosis causes hypertension but does not cause radiofemoral pulse delay or rib notching on imaging.

This newborn's presentation with severe cyanosis unresponsive to oxygen, a single S2, minimal murmur, and an "egg-on-a-string" silhouette is classic for transposition of the great arteries, where the aorta arises from the right ventricle and the pulmonary artery from the left ventricle, creating parallel rather than in-series circulations. Survival depends on mixing of oxygenated and deoxygenated blood, which occurs through the patent ductus arteriosus, foramen ovale, or septal defects. Intravenous prostaglandin E1 keeps the ductus arteriosus open, maintaining a mixing pathway and improving systemic oxygenation until balloon atrial septostomy or arterial switch surgery can be performed.

• A. Propranolol is used to prevent tet spells in tetralogy of Fallot, not to maintain ductal patency in TGA.
• B. Furosemide treats volume overload and heart failure, not the ductal-dependent mixing problem in TGA.
• C. Epinephrine is used in cardiac arrest or severe shock, not as initial management of ductal-dependent cyanotic heart disease.
• E. Indomethacin is a prostaglandin synthesis inhibitor used to close a PDA, which would worsen this ductal-dependent cyanotic lesion.

This child is having an uncomplicated vaso-occlusive pain crisis, the most common acute complication of sickle cell disease, caused by sickled erythrocytes obstructing microvascular flow and causing tissue ischemia. The priority is prompt, aggressive analgesia, typically with intravenous opioids such as morphine, along with IV hydration, because pain is often severe and undertreated. Transfusion is not indicated for an uncomplicated pain crisis with a hemoglobin at baseline and no evidence of acute chest syndrome, stroke, or severe anemia. Antibiotics and incentive spirometry are used when there is concern for infection or acute chest syndrome, which are not present here given clear lungs, normal oxygen saturation, and absence of fever or respiratory symptoms.

• A. Transfusion is reserved for severe anemia below baseline, acute chest syndrome, stroke, or splenic sequestration, none of which are present here.
• B. Incentive spirometry is used to prevent or treat acute chest syndrome, which is not suggested by this child's clear lungs and normal oxygen saturation.
• C. Exchange transfusion is reserved for severe complications like stroke or severe acute chest syndrome, not an uncomplicated pain crisis.
• E. Empiric antibiotics are indicated for fever or suspected infection, but this child is afebrile with no signs of infection.

Children with sickle cell disease have functional asplenia by early childhood, which markedly increases risk of overwhelming infection from encapsulated organisms, especially Streptococcus pneumoniae. Current guidelines recommend starting oral penicillin V prophylaxis by 2-3 months of age (dosing increases with age) and continuing through at least age 5 years, combined with the full pneumococcal conjugate vaccine (PCV) series on the standard schedule. The 23-valent pneumococcal polysaccharide vaccine is given later, at age 2 years and again at age 5, as a booster. These measures together substantially reduce mortality from pneumococcal sepsis in this population.

• A. Routine IVIG is not standard prophylaxis for infection prevention in sickle cell disease.
• B. Vaccinations should not be delayed in sickle cell disease; delay increases infection risk rather than reducing it.
• C. Splenectomy is not performed for prophylaxis in sickle cell disease and would worsen infection risk.
• E. Hydroxyurea does not substitute for infection prophylaxis, and the polysaccharide vaccine is not indicated at 6 months of age.

This infant has a positive Ortolani maneuver, suggesting developmental dysplasia of the hip (DDH), and she has an additional risk factor of breech presentation. In infants younger than 4-6 months, the femoral head and acetabulum are largely cartilaginous, so ultrasonography is the imaging modality of choice because it visualizes cartilage and allows dynamic assessment of hip stability. Plain radiographs become more useful after ossification occurs, typically around 4-6 months of age. Ultrasound findings guide the need for treatment with a Pavlik harness in confirmed DDH.

• B. Radiographs are unreliable before 4-6 months because the femoral head is not yet ossified.
• C. Arthrography is invasive and reserved for specific surgical planning, not initial screening.
• D. MRI is not first-line and typically requires sedation, offering no advantage over ultrasound in infants.
• E. CT is not used for DDH evaluation and involves unnecessary radiation exposure in infants.

Slipped capital femoral epiphysis (SCFE) classically occurs in obese adolescents aged 10-16 years and presents with groin, thigh, or knee pain, a limp, and limited internal rotation with obligate external rotation on hip flexion. In contrast, Legg-Calve-Perthes disease typically affects younger children (ages 4-10 years) and is not strongly associated with obesity. The absence of fever and the patient's age and body habitus make SCFE far more likely than an infectious or inflammatory process. Diagnosis is confirmed with anteroposterior and frog-leg lateral radiographs of the pelvis showing displacement of the femoral epiphysis.

• A. Juvenile idiopathic arthritis usually involves morning stiffness and joint swelling rather than this mechanical hip finding.
• C. The absence of fever and the chronic, insidious 3-week course argue against septic arthritis.
• D. Perthes disease occurs in younger children, typically 4-10 years old, and is not associated with obesity.
• E. Transient synovitis usually follows a viral illness and lacks the obligate external rotation sign typical of SCFE.

This child had a simple febrile seizure: a single generalized seizure lasting less than 15 minutes, with full recovery and no focal findings, occurring in a neurologically normal child between 6 months and 5 years. Management involves identifying and treating the source of fever, reassuring the family about the generally benign and self-limited nature of simple febrile seizures, and providing seizure first-aid education. Routine lumbar puncture, EEG, and neuroimaging are not indicated for a simple febrile seizure in a child who returns to baseline. Daily antiepileptic prophylaxis is not recommended because simple febrile seizures do not significantly increase the risk of future epilepsy.

• A. Lumbar puncture is only indicated if there are signs of meningitis, incomplete immunization status, or other concerning features, not routinely for a simple febrile seizure.
• B. Chronic antiepileptic therapy is not recommended for simple febrile seizures given their benign prognosis.
• C. Neuroimaging is unnecessary in a child with a simple febrile seizure and a normal neurologic examination.
• D. EEG is not indicated after a simple febrile seizure because it does not change management or predict recurrence.

Breath-holding spells occur in healthy toddlers, typically between 6 months and 6 years of age, and are triggered by crying from frustration, fear, or minor injury. In the pallid form, the child becomes pale and loses consciousness briefly, sometimes with brief stiffening, due to a vagally mediated reflex causing transient asystole or bradycardia, rather than a primary seizure disorder. The key distinguishing features from epileptic seizures are the clear emotional trigger, rapid and complete recovery, and normal interictal neurologic examination. Reassurance and parental education are the mainstay of management, and iron deficiency should be screened for since it can increase frequency of spells.

• A. Generalized tonic-clonic seizures are not consistently triggered by crying and typically have a longer postictal period.
• C. Long QT syndrome-related syncope is not classically triggered by crying after frustration and would need ECG evaluation if suspected, but this presentation is classic for a breath-holding spell.
• D. Infantile spells present with clusters of flexor spasms, usually in infants with developmental regression, which is not seen here.
• E. Absence seizures present with brief staring spells without a crying trigger or loss of tone, unlike this presentation.

This child has diabetic ketoacidosis (DKA) with dehydration, as shown by tachycardia, delayed capillary refill, hyperglycemia, ketonuria, and a high anion gap metabolic acidosis. Initial management is isotonic fluid resuscitation to restore perfusion, followed by a continuous intravenous insulin infusion (without a bolus, which increases risk of cerebral edema in children) to gradually correct hyperglycemia and halt ketogenesis. Potassium should be monitored closely and added to fluids once insulin is started, since insulin drives potassium intracellularly and total body potassium is typically depleted despite a normal or elevated initial serum level. Bicarbonate therapy is avoided in pediatric DKA because it increases the risk of cerebral edema without proven benefit.

• B. An initial insulin bolus is avoided in children with DKA because it increases the risk of cerebral edema and rapid osmotic shifts.
• C. Subcutaneous insulin and oral rehydration are inadequate for a child with significant dehydration and acidosis requiring intravenous therapy.
• D. Potassium should not be bolused; it is added to maintenance fluids after initial fluid resuscitation and with cardiac monitoring given this patient's already elevated level.
• E. Bicarbonate is not routinely given in pediatric DKA and increases the risk of cerebral edema.

This 46,XX infant has virilized external genitalia (ambiguous genitalia with labioscrotal fusion) and a salt-wasting adrenal crisis with hyponatremia, hyperkalemia, and hypoglycemia, the classic presentation of classic salt-wasting congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Loss of 21-hydroxylase blocks cortisol and aldosterone synthesis, shunting precursors toward androgen production, which virilizes a genetically female fetus in utero and causes aldosterone deficiency leading to salt wasting after birth. Diagnosis is confirmed by a markedly elevated serum 17-hydroxyprogesterone level. Management requires immediate IV fluids, dextrose, and stress-dose hydrocortisone, followed by lifelong glucocorticoid and mineralocorticoid replacement.

• B. This involves discordant gonadal development in individuals with sex chromosome mosaicism, not isolated virilization with a normal 46,XX karyotype.
• C. This causes undervirilization in 46,XY individuals, not virilization in 46,XX individuals, and does not cause salt wasting.
• D. This causes undervirilization in 46,XY individuals due to impaired testosterone synthesis, not virilization of a 46,XX fetus.
• E. This causes a 46,XY individual with female external genitalia due to androgen receptor defects, not virilization of a 46,XX fetus.

This child has nephrotic syndrome (heavy proteinuria, hypoalbuminemia, edema) with a presentation typical of minimal change disease, the most common cause of nephrotic syndrome in children aged 1-10 years, which is often preceded by a viral upper respiratory infection and does not show hematuria or hypertension. Because the clinical presentation is so characteristic, biopsy is not required before starting empiric therapy, and oral corticosteroids are first-line treatment. Most children achieve complete remission within 4-6 weeks of high-dose daily prednisone. Steroid-resistant or frequently relapsing disease may later require biopsy and second-line agents such as calcineurin inhibitors or cyclophosphamide.

• A. Diuretics can help manage edema symptomatically but do not treat the underlying glomerular disease.
• B. This is reserved for steroid-resistant or frequently relapsing disease, not first-line therapy for a new diagnosis.
• C. This is a second-line agent used for steroid-dependent or resistant nephrotic syndrome, not initial therapy.
• E. ACE inhibitors reduce proteinuria as adjunctive therapy but do not induce remission of minimal change disease on their own.

The 1-2 week latency between streptococcal pharyngitis and the onset of gross hematuria, hypertension, and edema, combined with red blood cell casts and an isolated low C3 with normal C4, is characteristic of post-streptococcal glomerulonephritis. This immune complex-mediated disease follows a predictable latency of 1-3 weeks after pharyngitis (or 3-6 weeks after impetigo), reflecting the time needed for antibody formation against streptococcal antigens deposited in the glomerular basement membrane. Complement levels typically normalize within 6-8 weeks, and most children recover renal function fully with supportive care alone. Diagnosis is supported by elevated anti-streptolysin O (ASO) titers or anti-DNase B antibodies.

• A. IgA nephropathy classically presents with gross hematuria within 1-3 days of a respiratory infection (synpharyngitic), not after a 2-week latency, and complement levels are normal.
• B. This hereditary disorder presents with persistent microscopic hematuria, sensorineural hearing loss, and a family history, not an acute post-infectious nephritic syndrome.
• D. This typically causes persistently low C3 beyond 8 weeks and a more chronic, progressive nephritic-nephrotic picture rather than a self-limited post-infectious course.
• E. This vasculitis presents with palpable purpura, arthralgia, and abdominal pain alongside nephritis, and complement levels are typically normal.

All infants diagnosed with Down syndrome should undergo an echocardiogram shortly after birth, regardless of whether a murmur is heard on examination, because congenital heart disease occurs in approximately 40-50% of affected infants and may be clinically silent initially. Atrioventricular septal defect is the most common lesion, followed by ventricular septal defect and secundum atrial septal defect. Early detection allows timely cardiology referral and surgical planning before pulmonary vascular disease develops. The American Academy of Pediatrics recommends this screening as part of routine health supervision for all newborns with Down syndrome.

• A. A skeletal survey is not a standard component of newborn screening for Down syndrome.
• B. Renal anomalies are not increased to the same degree in Down syndrome and are not part of universal newborn screening recommendations.
• C. Abdominal anomalies such as duodenal atresia are less common and are typically evaluated if symptoms such as bilious vomiting arise, not as universal screening.
• D. Routine brain imaging is not part of standard newborn screening for Down syndrome in an asymptomatic infant.