(Test Bank) Mcq 2022 American Academy Of Pediatrics

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2007 PREP SA on CD-ROM Question: 1 You are precepting a resident who has just evaluated a 4-year-old incompletely immunized immigrant boy who has classic varicella lesions and a history that is consistent with this diagnosis. Of the following, the MOST accurate statement is that A. lesions of both varicella and smallpox follow a 7- to 10-day course from eruption to resolution B. lesions of both varicella and smallpox frequently produce deep, pitted scars C. varicella lesions appear in stages or crops; smallpox lesions are uniformly in the same stage of development D. varicella lesions are concentrated on the face; smallpox lesions are concentrated over bony prominences E. varicella lesions are transient vesicles; smallpox lesions are persistent pustules until resolution of the illness Copyright © 2007 by the American Academy of Pediatrics page 12007 PREP SA on CD-ROM Preferred Response: C Critique: 1 Historically, the disease most often confused with severe varicella was smallpox. Smallpox, caused by the variola virus, a member of the orthopoxvirus family, has an incubation period of 7 to 17 days. During the incubation period, virus replicates in the upper respiratory tract. A primary viremia ensues, during which the liver and spleen are seeded. A secondary viremia follows, the skin is seeded, and the classic eruption appears. Initial symptoms of smallpox may include fever as high as 104°F (40°C), generalized malaise, severe headache, vomiting, and backache. Characteristic skin findings appear 1 to 2 days after the onset of fever. The rash begins on the face and then spreads to involve the extremities and trunk. Initially, lesions are erythematous macules; they evolve into papules, vesicles, and firm pustules (Item C1A). Crusts form at 8 or 9 days and persist for 3 to 4 weeks. As crusts separate, patients often are left with significant scars or depigmentation. Aspects of smallpox that differentiate it from severe varicella are that the majority of lesions are observed on the face and extremities (with lesser numbers on the trunk) and that all lesions are in a similar stage of development. In contrast, the lesions of varicella erupt initially on the trunk and later appear on the face and extremities. Lesions are erythematous papules that evolve to form superficial vesicles, pustules, and crusts. In varicella (unlike smallpox), lesions are observed in varying stages of development (ie, as older lesions crust, new lesions appear) (Item C1B). By 7 to 10 days after infection, all lesions have crusted. Permanent scars are rare, occurring only when lesions have been secondarily infected with bacteria. References: American Academy of Pediatrics. Smallpox (variola). In: Pickering LK, ed. Red Book: 2006 Report of the Committee on Infectious Diseases. 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006: 591-595 Cieslak J, Henretig FM. Biologic and chemical terrorism. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:2378- 2385 Myers MG, Stanberry LR, Sevard JF. Varicella-zoster virus. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, Pa: WB Saunders Co; 2004:1057-1062 Paller AS, Mancini AJ. Viral diseases of the skin. In: Hurwitz Clinical Pediatric Dermatology . 3rd ed. Philadelphia, Pa: Elsevier Inc; 2006: 397-423 Copyright © 2007 by the American Academy of Pediatrics page 22007 PREP SA on CD-ROM Question: 2 A 15-year-old boy presents with melena and anemia. Endoscopy demonstrates a nodular gastritis of the antrum (Item Q2A) and an ulcer. Biopsies of the antrum demonstrate spiral- shaped organisms consistent with Helicobacter pylori (Item Q2B). You prescribe amoxicillin, clarithromycin, and lansoprazole for 2 weeks. At a follow-up visit, the family asks whether the treatment has been successful in eradicating the organism. Of the following, the PREFERRED noninvasive test to evaluate whether the pathogen has been eradicated is A. fecal Campylobacter -like organisms (CLO) test B. fecal H pylori antigen C. salivary H pylori antibody concentrations D. serum H pylori immunoglobulin G serology E. serum H pylori urease concentrations Copyright © 2007 by the American Academy of Pediatrics page 32007 PREP SA on CD-ROM Preferred Response: B Critique: 2 Helicobacter pylori infection is a known risk factor for gastritis and duodenal ulcers in children and adults. Rarely, and primarily in older adulthood, H pylori also is associated with a gastric lymphoma of the mucosal-associated lymphoid tissue (MALToma). The “gold standard” for the diagnosis of H pylori infection of the stomach is endoscopy with biopsy. Endoscopy may show a nodular gastritis of the antrum (Item C2A), and histology of the gastric mucosa demonstrates the characteristic curved organisms (Item C2B) in the gastric glands. Because endoscopy is invasive, other surrogate markers of infection have been identified. Of the options offered, the H pylori fecal antigen is the best to document eradication in a previously treated host. Patients colonized with H pylori have detectable antigen in their stool that disappears upon eradication of the organism. H pylori immunoglobulin G serology (serum antibody) is a useful marker for epidemiologic studies of past or current infection, but its sensitivity and positive predictive value in children is suboptimal. The same is true for salivary antibody. Accordingly, a positive antibody screen should be confirmed by a second test (either fecal antigen, urea breath test, or endoscopy). The Campylobacter -like organisms (CLO) test is performed on a duodenal biopsy. In the CLO test, the duodenal biopsy specimen is placed in a test tube containing chemical reagents. The H pylori bacteria convert urea to ammonia and carbon dioxide via their urease enzyme, and the alkalinity of the ammonia can be detected using an indicator dye. The CLO test cannot be performed on feces. Serum urease concentrations are not helpful in identifying H pylori, which is a mucosal bacterium. Diagnosis, treatment, and eradication of H pylori are well summarized in the American Academy of Pediatrics Red Book and in the North American Society for Pediatric Gastroenterology practice guideline. Patients who have documented ulcers should be tested for H pylori and the organism eradicated if found, but it is unclear if asymptomatic children colonized with H pylori need to be treated. Therapy is given for 14 days and should include a proton pump inhibitor (eg, omeprazole, lansoprazole, pantoprazole) and two antibiotics (eg, tetracycline + clarithromycin, amoxicillin + metronidazole, amoxicillin + clarithromycin) (Item C2C). Treatment failures are common, either because of resistant bacteria or because of poor compliance with the regimen. Therefore, testing for eradication of the organism (either by fecal antigen, urease breath test, or endoscopy) should be performed more than 1 month after therapy has been completed. References: American Academy of Pediatrics. Helicobacter pylori infections. In: Pickering LK, ed. Red Book: 2006 Report of the Committee on Infectious Diseases . 27th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 2006:321-322 Gold BD, Colletti RB, Abbott M, et al. Helicobacter pylori infection in children: recommendations for diagnosis and treatment. J Pediatr Gastroenterol Nutr . 2000;31:490-497. Available at: http://www.jpgn.org/pt/re/jpgn/fulltext.00005176-200011000-00007.htm Copyright © 2007 by the American Academy of Pediatrics page 42007 PREP SA on CD-ROM Question: 3 A term newborn is delivered by emergent cesarean section because of intrauterine growth restriction, oligohydramnios, and nonreassuring fetal heart rate monitoring in labor. Delivery room resuscitation includes endotracheal intubation and assisted ventilation with 100% oxygen, chest compressions, intravenous epinephrine, and volume expansion. Apgar scores are 1, 2, and 3 at 1, 5, and 10 minutes, respectively. An umbilical cord arterial blood gas measurement documents a pH of 6.9 and a base deficit of 20 mmol/L. At 12 hours of age, the infant demonstrates tonic-clonic convulsive activity of the arms and legs with a concomitant decrease in heart rate and bedside pulse oximetry saturation. Of the following, the MOST likely cause for this infant's seizure is A. hypercalcemia B. hypercarbia C. hyperglycemia D. hypomagnesemia E. hypoxia Copyright © 2007 by the American Academy of Pediatrics page 52007 PREP SA on CD-ROM Preferred Response: E Critique: 3 Seizures are the most frequent sign of central nervous system injury in the newborn. When seizures occur in a newborn who has depressed neuromotor tone, reflexes, and cardiopulmonary function at birth that requires assisted ventilation, perinatal asphyxia is likely. In this event, Apgar scores typically are depressed to less than 3 at 5 or more minutes after birth, and there is a severely acidotic umbilical cord arterial pH (<7.0), with evidence of metabolic acidemia. Poor tolerance of labor and asphyxia are more common in fetuses that have experienced intrauterine growth restriction. Because the infant in the vignette has the previously described features, hypoxic-ischemic encephalopathy (HIE) must be considered as a cause for the seizures. HIE is the most common cause of seizures occurring in the first 24 hours of postnatal life and accounts for up to 67% of early neonatal seizures. Other causes of neonatal seizure include intracranial hemorrhage, cerebrovascular accidents (stroke), or hemorrhagic infarction (10% to 15%); intracranial malformation (<10%); transient hypoglycemia or hypocalcemia (<10%); drug withdrawal (<5%); and inborn errors of metabolism (<5%). When seizures occur beyond the first 24 hours after birth, especially in the absence of any history of fetal or neonatal asphyxia, the evaluation should focus on potential causes other than HIE. An additional cause for later seizures is infection (meningitis, encephalitis). Asphyxia may result in hypocalcemia and hypoglycemia; hyperglycemia and hypercalcemia are not associated with HIE and do not typically cause seizures. Hypomagnesemia may accompany hypocalcemia in the infant of a diabetic mother, but it is not common following asphyxia and is not associated with neonatal seizures. Hypercarbia may occur in the depressed newborn who has inadequate ventilation, but it is not associated with seizures unless there is corresponding hypoxia. References: Allan WC. The clinical spectrum and prediction of outcome in hypoxic-ischemic encephalopathy. NeoReviews. 2002;3:e108-e115. Available at: http://neoreviews.aappublications.org/cgi/content/full/3/6/e108 Hahn JS, Olson DM. Etiology of neonatal seizures. NeoReviews. 2004;5:e327-e335. Available at: http://neoreviews.aappublications.org/cgi/content/full/5/8/e327 Riviello JJ, Jr. Pharmacology review: drug therapy for neonatal seizures: part 2. NeoReviews. 2004;5:e262-e268. Available at: http://neoreviews.aappublications.org/cgi/content/full/5/6/e262 Thureen PJ, Anderson MS, Hay WW, Jr. The small-for-gestational age infant. NeoReviews. 2001;2:e139-e149. Available at: http://neoreviews.aappublications.org/cgi/content/full/2/6/e139 Wu YW, Backstrand KH, Zhao S, Fullerton HJ, Johnston SC. Declining diagnosis of birth asphyxia in California: 1991-2000. Pediatrics. 2004;114:1584-1590. Available at: http://pediatrics.aappublications.org/cgi/content/full/114/6/1584 Copyright © 2007 by the American Academy of Pediatrics page 62007 PREP SA on CD-ROM Question: 4 A 2-year-old boy presents with a 3-day history of diarrhea and vomiting. He has been able to tolerate small amounts of fluids. He is moderately dehydrated, with dry mucous membranes and a heart rate of 145 beats/min. Of the following, the BEST management for this patient's fluid status is A. hospitalization with intravenous fluids and a restrictive bland diet B. hospitalization with intravenous fluids and gut rest for 24 hours C. oral rehydration therapy at home followed by a clear liquid diet for 24 hours D. oral rehydration therapy at home followed by a diet of fruits, vegetables, and meats E. oral rehydration therapy at home followed by a restrictive bland diet Copyright © 2007 by the American Academy of Pediatrics page 72007 PREP SA on CD-ROM Preferred Response: D Critique: 4 Dehydration results from a total body loss of water and sodium. Acute infectious gastroenteritis is among the most common causes of dehydration in infants and young children. Both mild and moderate dehydration may be managed at home with oral rehydration therapy, even if the child continues to have intermittent vomiting. Commercial oral rehydration solutions (ORS) are widely available and should be used for this purpose. All ORS are designed to replace lost electrolytes (sodium, chloride, potassium, and bicarbonate) glucose, and water. Young children who have mild dehydration have an estimated water loss of 50 mL/kg, and this amount of ORS can be given via a spoon or syringe in small amounts over 2 to 4 hours. Those who have moderate dehydration should receive 100 mL/kg over 2 to 4 hours. Care should be taken to monitor ongoing losses from stool and emesis, and intravenous or nasogastric rehydration therapy should be considered if losses are excessive or if dehydration worsens or does not improve. Oral rehydration therapy should not be used for children who have severe dehydration, shock, suspected intestinal obstruction, obtundation, or ileus. Once adequate hydration has been assured or rehydration is complete, a normal diet should be given to the child to ensure adequate caloric and nutrient intake. A period without gastrointestinal intake is unnecessary and may delay nutritional recovery. Clear liquid and bland diets also should not be used because they do not provide adequate nutrition. Infants should be given human milk or their usual formula at full strength because diluted formula or human milk (eg, one-half or one-quarter strength formula) will not meet the child’s caloric requirements and may worsen electrolyte abnormalities. Lactose-free formulas are generally unnecessary because most children do not develop lactase deficiency. Older children should be given a regular diet of complex carbohydrates, fruits, vegetables, and meats. High sugar-containing liquids should be avoided because the osmotic load of these liquids may worsen diarrhea. References: Finberg L. Dehydration in infancy and childhood. Pediatr Rev. 2002;23:277-282. Available at: http://pedsinreview.aappublications.org/cgi/content/full/23/8/277 King CK, Glass R, Bresee JS, Duggan C, Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep . 2003;52(RR-16):1-16. Available at: http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5216a1.htm Copyright © 2007 by the American Academy of Pediatrics page 82007 PREP SA on CD-ROM Question: 5 A worried grandmother brings her 2-year-old grandchild to the emergency department immediately upon finding the boy with an open bottle of 81-mg chewable aspirin (which is used by the grandfather for coronary artery disease prophylaxis). She is unsure of the number of tablets in the bottle prior to ingestion, but the original number was 30, and there are now three remaining. The child has vomited once and is fussy and lethargic. Physical evaluation reveals a 12-kg child who has tachypnea and tachycardia. Laboratory results include a pH of 7.45, carbon dioxide of 25 mEq/L (25 mmol/L), and bicarbonate of 18 mEq/L (18 mmol/L). A salicylate measurement result is pending. Of the following, the next BEST step in the management of this child is to A. administer activated charcoal B. administer sodium bicarbonate intravenously C. administer syrup of ipecac D. observe the child clinically in the emergency department E. remeasure the salicylate level in 6 hours Copyright © 2007 by the American Academy of Pediatrics page 92007 PREP SA on CD-ROM Preferred Response: A Critique: 5 Salicylates are common in the homes of many children because many older adults (who may be parents or grandparents) use salicylates for prophylaxis against cardiovascular disease and for arthritis pain. Methylsalicylate present in liniments is especially concentrated. The toddler may ingest such preparations accidentally, as described for the boy in the vignette, and the adolescent may use salicylates in suicide gestures or attempts. Toxic effects of salicylates can include gastritis, anticoagulant effects, increased metabolism, hyperventilation and respiratory alkalosis, and hepatitis. Reye syndrome, which is characterized by hepatitis and encephalopathy, may occur if aspirin is given during certain viral infections. Signs and symptoms include lethargy or coma, vomiting, tachypnea, and tachycardia. The next best step in the management of the child described in the vignette is the administration of activated charcoal. Multiple doses of activated charcoal adsorb salicylates from both the intestinal tract and the systemic circulation. For a child who has ingested a potentially toxic dose of salicylates, serum salicylate concentrations should be measured 2 to 6 hours after the ingestion. However, administration of activated charcoal should not be delayed until the salicylate concentration has been measured if a toxic dose has been ingested. The child in the vignette may have ingested 27 81-mg tablets for a total dose of more than 2,100 mg or 182 mg/kg. This dose can be expected to cause mild-to- moderate toxicity. A serum salicylate value higher than 30 mg/dL is considered toxic, concentrations higher than 70 mg/dL reflect severe toxicity, and those greater than 100 mg/dL are life-threatening. Because gastric emptying time is prolonged with salicylate ingestion, gastrointestinal decontamination by lavage may be effective up to 6 hours after ingestion. However, the child described in the vignette is fussy and lethargic. Therefore, syrup of ipecac is not indicated. Administration of sodium bicarbonate to alkalinize the urine as well as correction of acidosis, hyperkalemia, and hypocalcemia are important adjuncts to gastric decontamination. Cautious administration of intravenous sodium bicarbonate may be indicated clinically in severe acidosis because acidosis enhances brain toxicity, but the patient must be monitored for worsening hypernatremia and hypokalemia as a response to alkalinization. Although the child in the vignette should be observed and repeat salicylate concentrations obtained, gastrointestinal decontamination with activated charcoal is therapeutic and, thus, the next best step. References: Mariscalco MM. Salicylism. In: McMillin JA, DeAngelis CD, Feigin RD, Warshaw JB, eds. Oski’s Pediatrics: Principles and Practice . 3rd ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 1999:623-625 Woolf AD. Poisoning in children and adolescents. Pediatr Rev . 1993;14:411-422 Copyright © 2007 by the American Academy of Pediatrics page 102007 PREP SA on CD-ROM Question: 6 A mother brings her 10-month-old son to the emergency department because he has been vomiting for the past 10 days. The child has not experienced any diarrhea. On physical examination, he is lethargic and has dry mucous membranes, reduced tears, a full anterior fontanelle, and 2-second capillary refill. After a second intravenous bolus of 20 mL/kg of normal saline, the boy extends his arms and legs forcefully for 10 seconds. Of the following, the MOST appropriate next step in the management of this child is administration of A. additional intravenous normal saline bolus of 20 mL/kg B. intravenous dexamethasone of 1 mg/kg C. intravenous fosphenytoin bolus at 20 mg/kg phenytoin equivalents over 10 minutes D. intravenous prochlorperazine of 5 mg E. rapid intravenous lorazepam of 0.05 mg/kg Copyright © 2007 by the American Academy of Pediatrics page 112007 PREP SA on CD-ROM Preferred Response: B Critique: 6 Brain tumors occur rarely in the pediatric population; the incidence is just under 1 in 25,000 children annually. Despite its rarity, the ominous nature of such a diagnosis requires that practitioners be able to recognize readily the clinical manifestations of a brain tumor. Clinical prodromes may include features of increased intracranial pressure (ICP) (Item C6A), findings of a localizing nature, or symptoms and signs without a localizing quality. Elevated ICP often is insidious and nonspecific initially. Among school-age children, declining academic performance, fatigue, behavioral changes, and vague intermittent headaches are common. Over time, morning headaches, especially pain at the occipital or frontal region, along with vomiting and lethargy ensue. Horizontal diplopia from abducens nerve paresis is common. Papilledema may develop if the pressure is longstanding. Among infants, irritability, anorexia, failure to thrive, and even developmental regression can be early signs of increased ICP. Macrocephaly, splitting of the cranial sutures, or a bulging anterior fontanelle can follow. The “setting sun” sign, a downward deviation of the eyes, may be seen with attendant hydrocephalus. Localizing findings depend on the region of the brain involved. Supratentorial (cerebrum, basal ganglia, thalamus, hypothalamus, and optic chiasm) tumors can produce hemiparesis, hemisensory loss, hyperreflexia, seizures, or visual complaints. Infratentorial (cerebellum and brainstem) tumors lead to ataxia, hemiparesis, hyperreflexia, or cranial neuropathies, but not seizures. Nonlocalizing symptoms and signs are perhaps the most subtle manifestations of a brain tumor. The child may display changes in affect, energy level, behavior, or weight. Sexual precocity or delayed puberty, growth failure, and somnolence can suggest hypothalamic or pituitary dysfunction. Vomiting can occur with direct irritation of the area postrema in the floor of the fourth ventricle or from a generalized increase in ICP. The vomiting without diarrhea displayed by the 10-month-old in the vignette, along with a full anterior fontanelle in the face of mild dehydration, points to an intracranial process. In addition, the child is exhibiting posturing, not a seizure, from continued overhydration and worsening intracranial pressure following the saline administration. Accordingly, administration of intravenous dexamethasone, along with other measures to treat increased ICP, is most appropriate. Treatment with prochlorperazine will only mask the child’s vomiting. Administration of fosphenytoin or lorazepam is not indicated in the absence of seizures. Continued aggressive hydration will worsen this child’s ICP. References: Kuttesch JF Jr, Alter JL. Brain tumors in childhood. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson Textbook of Pediatrics . 17th ed. Philadelphia, Pa: WB Saunders; 2004:1702-1708 Strother DR, Pollock IF, Fisher PG, et al. Tumors of the central nervous system. In: Pizzo PA, Poplack DG, eds. Principles and Practice of Pediatric Oncology . 4th ed. Philadelphia, Pa: Lippincott, Williams & Wilkins; 2002:751-824 Copyright © 2007 by the American Academy of Pediatrics page 122007 PREP SA on CD-ROM Question: 7 An 18-month-old child has been brought to your urgent care clinic for evaluation. He and his mother are in town visiting his grandmother. His mother tells you that she found him playing with an open bottle of his grandmother's medication. On physical examination, he is sleepy but arousable, pale, mildly diaphoretic, and afebrile. His respiratory rate is 20 breaths/min, heart rate is 60 beats/min, and blood pressure is 65/40 mm Hg. His lungs are clear, there are no murmurs, and his pulses are weak. Of the following, the MOST likely cause for this patient's presentation is ingestion of A. beta blocker B. captopril C. hydralazine D. pseudoephedrine E. tricyclic antidepressant Copyright © 2007 by the American Academy of Pediatrics page 132007 PREP SA on CD-ROM Preferred Response: A Critique: 7 Accidental ingestion of medications continues to be a significant cause of pediatric morbidity and potential mortality. The problem is greatest in toddlers and is exacerbated when medications are left within reach of children or not appropriately secured in a locked cabinet. The reaction to ingestion of a given medication depends on the class and dose. Beta blockers can have multiple and varying effects on the heart and other organ systems. In the heart, they typically exhibit some degree of negative chronotropic (slowing of the heart rate), dromotropic (slowing of the conduction through the AV node), and inotropic (decrease in the ventricular force of contraction) effects. As a result, this class of medications generally is used to control certain types of arrhythmia and hypertension and to reduce myocardial work and oxygen demand. The depressed sensorium, bradycardia for age, and hypotension with diminished pulses described for the child in the vignette are most consistent with beta blocker ingestion. Captopril is an angiotensin-converting enzyme (ACE) inhibitor. ACE activity converts angiotensin I to angiotensin II, which is a potent vasoconstrictor. Therefore, ACE inhibitors lower the systemic vascular resistance and the systemic blood pressure, decreasing the afterload (work) of the left ventricle. Hydralazine is an arteriolar dilator that may have some positive inotropic effect. It often is used as antihypertensive therapy and typically increases the heart rate. Pseudoephedrine is an alpha agonist that is used commonly for relief of symptoms caused by nasal congestion. Its effects on the cardiovascular system are to cause systemic vasoconstriction that may increase blood pressure, and it also may cause tachycardia. Tricyclic antidepressants are a diverse group of medications that can be used for a variety of noncardiac indications, including depression. When taken in high doses, they may affect the cardiovascular system by causing vasodilation, flushing, hypotension, and tachyarrhythmias. Although captopril, hydralazine, and tricyclic antidepressants may be associated with hypotension, they all would be expected to cause (or be associated with) a corresponding tachycardia. References: Dobson JV, Webb SA. Life-threatening pediatric poisonings. J S C Med Assoc . 2004;100:327- 332. Abstract available at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_ui ds=15835193&query_hl=11&itool=pubmed_docsum Opie L, Gersh B. Drugs for the Heart . 6th ed. Philadelphia, Pa: WB Saunders Co; 2004 Riordan M, Rylance G, Berry K. Poisoning in children 1: general management. Arch Dis Child . 2002;87:392-396. Available at: http://adc.bmjjournals.com/cgi/content/full/87/5/392 Copyright © 2007 by the American Academy of Pediatrics page 142007 PREP SA on CD-ROM Question: 8 The parents of a child who has Down syndrome and a 47,XX+21 karyotype come to you for counseling about future pregnancies. Of the following, their risk for giving birth to another child who has trisomy is CLOSEST to A. no greater than the general population at risk B. 1% added to the mother's age-related risk C. 5% added to the mother's age-related risk D. 10% added to the mother's age-related risk E. 25% added to the mother's age-related risk Copyright © 2007 by the American Academy of Pediatrics page 15