MCQ 2007 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

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2007 PREP SA on CD-ROM Critique: 1

Preferred Response: C

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; 2004:23782385 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

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2007 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 spiralshaped 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

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2007 PREP SA on CD-ROM Critique: 2

Preferred Response: B

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

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2007 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

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2007 PREP SA on CD-ROM Critique: 3

Preferred Response: E

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 (