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2002 Self-Assessment Exercise —
II. Nutrition and nutritional disorders
[Return to Category List]

Questions

Question 15. Answer.

You are discussing with a medical student the factors affecting the energy requirements of a
preterm neonate.
Of the following, the MOST accurate statement about energy expenditure of a preterm infant
is that:
A. a thermoneutral environment is effective in minimizing energy expenditure
B. diet-induced thermogenesis is higher with continuous than with intermittent feeding
C. metabolic cost of growth is higher with deposition of fat than with synthesis of
protein
D. physical activity is the major component of total energy expenditure
E. resting metabolic rate decreases with advancing postnatal age

Question 52. Answer.

The mother of a 12-year-old boy who is new to your practice is concerned about her son's
milk allergy. At age 7, he developed symptoms of abdominal pain, bloating, and flatulence
after ingesting milk. He never has been evaluated formally for the allergy, but his mother has
been having him avoid milk products to be safe. The child admits that he occasionally eats
ice cream at school without problems and only has symptoms if he consumes a large amount.
Of the following, the MOST appropriate course of action is to:
A. allow the child to eat only lactose-free dairy products
B. evaluate the child for milk allergy
C. have the child avoid all milk products diligently
D. have the family reintroduce milk products gradually at home
E. prescribe injectable epinephrine to the patient

Question 95. Answer.

A 6-year-old child who has chronic liver disease becomes disoriented and develops vomiting,
nausea, and weakness. She is receiving fat-soluble vitamin replacement therapy. Evaluation
reveals hypercalcemia, hypercalciuria, and osteopenia.
Of the following, the MOST likely cause of this girl's symptoms is:

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A. hypervitaminosis A
B. hypervitaminosis D
C. vitamin A deficiency
D. vitamin E deficiency
E. vitamin K deficiency

Question 142. Answer.

A high school student wants to know why the American Academy of Pediatrics has
recommended exclusive breastfeeding during the first 6 months of life and continuation
through the second 6 months. Her research resources indicate that cow milk formula has 40%
more protein than human milk.
Your discussion about the protein in human milk compared with cow milk formula is MOST
likely to include information that mature human milk:
A. feeding results in higher serum concentrations of methionine
B. feeding results in higher serum concentrations of valine
C. has the same concentration of protein as cow milk-based formula
D. protein delays gastric emptying
E. whey proteins have more lactoferrin and secretory immunoglobulin A

Question 172. Answer.

A severely malnourished 10-year-old boy develops respiratory distress shortly after total
parenteral nutrition with 20% dextrose is initiated. His fluid intake is appropriate for his
weight and hydration syndrome.
Of the following, the MOST likely cause of his respiratory distress is:
A. excessive carbohydrate administration
B. excessive lipid administration
C. excessive protein administration
D. inadequate bicarbonate administration
E. inadequate calcium administration

Question 216. Answer.

You are evaluating a 2-month-old male infant who presented with irritability, protracted
vomiting, and diarrhea. He presently is receiving a milk-based formula. You suspect that
these symptoms may be food-induced, even though the patient had negative results on skin
testing for cow milk protein. You suggest changing to an elemental formula because he also
may be allergic to soy protein.
Of the patients who have milk protein allergy, the percentage who also have soy protein
allergy is CLOSEST to:
A. 10% to 20%
B. 20% to 30%
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C. 40% to 50%
D. 70% to 80%
E. 80% to 90%

Question 251. Answer.

A 4-year-old boy who has suffered cerebral anoxia due to a near-drowning episode is
malnourished. He has had four episodes of pneumonia. Although there is no family history of
asthma, he also has had episodes of wheezing.
Of the following, the MOST likely cause of his chronic lung disease is:
A. environmental allergies
B. gastroesophageal reflux
C. immotile cilia syndrome
D. interstitial pneumonitis
E. reactive airway disease

Answers

Critique 15. Preferred Response: A

[View Question]
The preterm neonate’s energy expenditure can be minimized by keeping the infant in a
thermoneutral environment. The thermoneutral environment is a range of ambient
temperatures within which the metabolic rate of the infant is minimal and the infant can
maintain a normal body temperature without any regulatory changes in metabolic heat
production or evaporative heat loss. The thermoneutral range varies with gestational age. In
an unclothed resting adult, the lower limit of the thermoneutral range is 78.8°F to 82.4°F
(26°C to 28°C) in an environment of 50% relative humidity and still air. Under similar
conditions, the lower limit of the thermoneutral range is 89.6°F (32°C) or higher in a naked
term neonate and 95°F (35°C) or higher in a naked preterm neonate.
Diet-induced thermogenesis, also known as specific dynamic action, thermic effect of
food, or postprandial thermogenesis, is the increase in metabolic rate that follows food intake.
It represents the energy consumption necessary for digestion, absorption, and assimilation of
nutrients. The magnitude of increase in energy expenditure following the ingestion of
nutrients is estimated to vary between 4% and 30% in both term and preterm neonates.
Diet-induced thermogenesis is lower with continuous than with intermittent enteral feeding.
Metabolic cost of growth represents the energy required for the formation of new
tissue, and it varies with the composition of the synthesized tissue. The cost of depositing
absorbed dietary fat into adipose tissue is much less than that of synthesizing new protein.
The overall metabolic cost of growth in neonates is estimated at approximately 4.4 kcal/g of
weight gain.
Energy expenditure increases with physical activity, but because neonates sleep 80%
to 90% of the time, physical activity is a small component of their energy expenditure
compared with that of adults. It is estimated that physical activity contributes to only about
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10% of the total energy expenditure in preterm neonates.
Resting metabolic rate increases steadily from birth in both term and preterm
neonates. The resting metabolic rate in term neonates is estimated at approximately 40
kcal/kg per day at 3 days of postnatal age, increasing to approximately 60 kcal/kg per day at
3 months of postnatal age. A similar but smaller increase in resting metabolic rate is observed
in preterm neonates.
References:
Brück K. Neonatal thermal regulation. In: Polin RA, Fox WW, eds. Fetal and Neonatal
Physiology. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1998:676-702
Leitch CA, Denne SC. Energy expenditure in the extremely low-birth weight infant. Clin
Perinatol. 2000;27:181-195

Critique 52. Preferred Response: A

[View Question]
When a child has gastrointestinal symptoms after ingesting dairy products, a careful history is
necessary to determine if the symptoms are due to milk protein allergy or lactose intolerance.
A milk protein allergy is an immunoglobulin E (IgE)-mediated event, with symptoms ranging
from mild abdominal pain, vomiting, and diarrhea to anaphylaxis and even death. Milk
proteins also have been associated with exacerbations of atopic dermatitis. These reactions
usually occur initially when the child is younger than 2 years of age, and symptoms may be
triggered by the ingestion of even minute amounts of diary products. In fact, the only
quantitative association in food allergy is that ingestion of larger quantities can lead to more
significant reactions.
Lactose intolerance is caused by a deficiency of the enzyme lactase that breaks down
lactose, a disaccharide, into the monosaccharides, glucose and galactose. If lactose is not
appropriately digested, symptoms of abdominal pain, flatulence, and bloating occur, as
described for the child in the vignette. Because most children who have lactose intolerance
usually have some lactase, the occasional ingestion of small amounts of lactose does not
elicit a reaction. In contrast, the child who has milk protein allergy often cannot tolerate even
minute amounts of milk product.
Evaluating the boy in the vignette for milk protein allergy probably is unnecessary
because he admits to ingestion of milk-containing foods without consequences. Placing the
child on a lactose-free diet not only can be therapeutic, but it also can be diagnostic.
Avoiding milk protein entirely or carefully reintroducing milk products is not necessary; it is
lactose that should be avoided or appropriate supplemental lactase should be used. The child
does not require an epinephrine prescription because lactose intolerance does not have an
anaphylactic potential.
References:
Sampson HA. Adverse reactions to foods. In: Middleton E Jr, Reed CE, Ellis EF, Adkinson
NF Jr, Yunginger JW, Busse WW, eds. Allergy: Principles and Practice. 5th ed. St Louis,
Mo: Mosby-Year Book, Inc; 1998:1162-1182
Sampson HA. Food allergy. JAMA. 1997;278:1888-1894
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Sly M. Adverse reactions to foods. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson
Textbook of Pediatrics. 16th ed. Philadelphia, Pa: WB Saunders Co; 2000:695-697

Critique 95. Preferred Response: B

[View Question]
Patients who have chronic liver and renal disease routinely receive supplemental fat-soluble
vitamin therapy, including vitamin D. Excessive amounts of vitamin D result in signs and
symptoms similar to those of idiopathic hypercalcemia, including hypotonia, anorexia,
irritability, constipation or diarrhea, polydipsia, and polyuria. Hypercalcemia and
hypercalcuria often are noted, as in the girl described in the vignette. Vomiting, poor growth,
osteopenia, and hypertension also may develop. Prolonged ingestion of excessive vitamin D
may result in renal damage due to nephrocalcinosis. Metastatic calcification of the heart,
blood vessels, bronchi, and stomach also may occur.
The body’s vitamin D requirements are met through its production in the skin, the
photochemical reaction of sunlight upon its precursor, and dietary ingestion. The primary role
of the vitamin is to stimulate absorption of calcium and phosphorus from the small intestine.
Children who have dark pigmented skin or limited exposure to the sun are at risk for vitamin
D deficiency. Anticonvulsant therapy may alter vitamin D metabolism, resulting in a
deficiency state. Human milk is normally low in vitamin D content, placing the exclusively
breastfed infant at risk if the mother’s vitamin D intake is suboptimal.
The metabolism of the fat-soluble vitamins A, D, E, and K differ from that of
water-soluble vitamins in several respects. First, their absorption depends on normal
pancreatic and hepatobiliary function. Second, they require a transport system to become
soluble in blood. Third, there is significant storage of these vitamins in the body, making
primary deficiency syndromes uncommon in healthy individuals. Finally, there is a potential
for toxicity if excessive fat-soluble vitamin ingestion occurs over a prolonged period of time.
Hypervitaminosis A is associated with anorexia, slow growth, hepatosplenomegaly,
swelling and pain of the long bones, increased intracranial pressure, and alopecia. Although
many of the symptoms resemble those seen with vitamin D toxicity, hypercalciuria and
hypercalcemia do not occur. Vitamin A deficiency causes photophobia, xerophthalmia, faulty
epiphyseal bone formation, retarded growth, and decreased resistance to infection.
Patients who have vitamin E deficiency develop red blood cell hemolysis, loss of
neural integrity, and decreased muscle function. Vitamin K deficiency results in soft-tissue
hemorrhage and defective bone collagen production.
References:
American Academy of Pediatrics Committee on Nutrition. Vitamins and mineral supplement
needs of healthy children in the United States. In: Barness LA, ed. Pediatric Nutrition
Handbook. 3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1993:34-42
Forbes GB, Cafarelli C, Manning J. Vitamin D and infantile hypercalcemia. Pediatrics.
1968;42:203-204

Critique 142. Preferred Response: E

[View Question]
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There are differences in both the quantity and quality of protein content in human and cow
milk. The protein concentration of mature human milk is 0.9 g/dL compared with 3.4 g/dL
for cow milk and 1.5 g/dL for modified cow milk formulas that provide 20 kcal/oz. The
protein content of human milk is 70% whey and 30% casein; cow milk contains 18% whey
and 82% casein. The various modified cow milk formulas have whey contents that vary from
18% to 100%. The predominant whey protein of human milk is alpha lactalbumin and is beta
lactoglobulin in cow milk. The whey proteins of human milk provide relatively greater
amounts of lactoferrin, lysozyme, and secretory immunoglobulin A than are contained in cow
milk formulas.
The serum levels of methionine, phenylamine, threonine, and valine are higher in
infants fed whey-dominant modified cow milk formulas compared with breastfed infants.
There is no known adverse effect associated with these differences.
The whey proteins, which are more plentiful in human milk, are digested more easily
and promote gastric emptying.
References:
Hall RT, Carroll RE. Infant feeding. Pediatr Rev. 2000;21:191-199
Slusser W, Powers NG. Breastfeeding update l: immunology, nutrition, and advocacy.
Pediatr Rev. 1997;18:111-119

Critique 172. Preferred Response: A

[View Question]
Patients who require parenteral nutrition often are moderately or severely malnourished.
Aggressive use of intravenous or enteral nutrition can result in mineral and metabolic
abnormalities (hypophosphatemia, hypokalemia, hypoglycemia, hypomagnesemia,
hypocalcemia) that lead to respiratory, neuromuscular, cardiac, and hematologic dysfunction,
termed refeeding syndrome. In response to chronic undernutrition, there may be
compensatory reductions in cardiac output, hemoglobin level, muscle mass, hepatic glycogen
content, and renal concentrating ability. Refeeding syndrome occurs when energy substrates,
particularly carbohydrate, are initiated in a catabolic patient. The resulting hyperinsulinemia
stimulates intracellular uptake of glucose, potassium, phosphorus, and magnesium to support
the proliferating body cell mass and hepatic glycogen synthesis.
Excessive carbohydrate administration can result in respiratory failure, as noted for
the boy in the vignette. If the amount of carbon dioxide produced during metabolism of the
carbohydrate exceeds the ventilatory capacity, the Pco2 will increase, especially in patients
who have underlying pulmonary disease. Water overload, which can result from salt and
water retention following the increased insulin concentrations, also is associated with
excessive carbohydrate administration. Increased metabolic rate and cardiac workload can
lead to congestive heart failure, especially if the left ventricle has been thinned by
malnutrition. Although excessive fluid administration can result in congestive heart failure in
a malnourished patient, fluids alone do not cause the refeeding syndrome. Careful attention to
fluid and calorie administration will help to prevent the refeeding syndrome. Using an
alternate source of calories (fat), the metabolism of which produces less carbon dioxide, and
supplementation with magnesium, potassium, and phosphorus also will decrease the
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likelihood of refeeding syndrome developing.
On an equimolar basis, lipid metabolism produces less carbon dioxide than does
carbohydrate and is, therefore, less likely to cause the respiratory failure associated with the
refeeding syndrome. Although acidosis and hypocalcemia can develop in patients receiving
parenteral nutrition, they are not associated with the development of respiratory failure in the
absence of tetany. Excessive protein intake does not have any effect on respiratory function.
References:
Nichols BL, Alvarado J, Rodriguez J, Hazlewood CF, Viteri F. Therapeutic implications of
electrolyte, water, and nitrogen losses during recovery from protein-calorie malnutrition. J
Pediatr. 1974;84:759-768
Solomon SM, Kirby DF. The refeeding syndrome: a review. J Parenter Enteral Nutr.
1990;14:90-97

Critique 216. Preferred Response: C

[View Question]
The incidence of cross-reactivity between milk protein allergy and soy protein allergy is
closest to 40% to 50%. Patients who have significant intolerance to cow milk are especially
likely to also have soy protein allergy. Clinical manifestations of soy or cow milk protein
allergy include gastrointestinal and possibly respiratory symptoms. The symptoms differ
from those seen in anaphylaxis in that they are associated with other findings, such as oral
ulcers, hemorrhagic gastric mucosa, and acute and chronic diarrhea. Most patients become
hypoproteinemic and anemic because of protein and blood losses through the gastrointestinal
tract. Failure to thrive and metabolic acidosis due to loss of bicarbonate also may occur.
Avoiding the offending antigen decreases symptoms in affected patients within 48
hours, with almost complete improvement within 1 week. An avoidance diet is not only
diagnostic, but also therapeutic. In the breastfed child who is allergic to soy and/or cow milk
protein, an elimination diet for the mother sometimes is successful in eliminating the infant’s
symptoms, but in other cases weaning may be necessary. Results of skin testing and
radioallergosorbent testing for cow or soy milk are not always positive.
References:
Sampson HA. Adverse reactions to foods. In: Middleton E Jr, Reed CE, Ellis EF, Adkinson
NF Jr, Yunginger JW, Busse WW, eds. Allergy: Principles and Practice. 5th ed. St Louis,
Mo: Mosby-Year Book, Inc; 1998:1162-1182
Sampson HA. Food allergy. JAMA. 1997;278:1888-1894
Sly M. Adverse reactions to foods. In: Behrman RE, Kliegman RM, Jenson HB, eds. Nelson
Textbook of Pediatrics. 16th ed. Philadelphia, Pa: WB Saunders Co; 2000:695-697

Critique 251. Preferred Response: B

[View Question]
As many as 44% of term infants have some degree of gastroesophageal reflux (GER) during
infancy. In most, GER is due to incompetence or inappropriate relaxation of the lower
esophageal sphincter. In rare instances, it is associated with more generalized motility
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disorders of the gastrointestinal tract or esophageal atresia. Symptoms are manifested within
the first 6 weeks of life in 95% of infants, with a majority developing reflux symptoms during
the first week of life. Although the emesis characteristically is nonprojectile and nonbilious,
infants who have delayed gastric emptying due to pylorospasm may have projectile vomiting
that suggests the diagnosis of pyloric stenosis. In most infants, GER is of little clinical
significance (ie, physiologic reflux) and requires neither diagnostic evaluation nor
pharmacologic intervention. Typically GER resolves before 18 months of age.
The incidence of GER is much higher in children who are neurologically impaired
than in the general population. As many as 75% of neurologically impaired children vomit
regularly, and GER is diagnosed in 75% of those who vomit. The symptoms of GER in this
population are similar to those seen in neurologically intact children, including recurrent
aspiration pneumonia, reactive airway disease and wheezing, stridor, croup, and hoarseness.
Excessive crying or atypical colic and Sandifer syndrome (an unusual posturing of the head
associated with intraesophageal acidification) may be the only clinical manifestations.
Nutritional consequences of GER include failure to thrive due to excessive caloric losses
through regurgitation, feeding refusal because of esophagitis, or protein-losing enteropathy
associated with severe esophagitis. Based on the history and symptoms, the boy described in
the vignette fits the profile of a neurologically impaired child who has GER.
The risk of Barrett esophagus, a premalignant lesion characterized by replacement of
esophageal squamous epithelium with specialized columnar metaplasia, also is much higher
in the neurologically impaired child who has GER. Many of these children have autonomic
neuropathy, which results in a prolonged esophageal transit time and a low basal lower
esophageal sphincter pressure. Finally, the natural history of GER in this population is
protracted.
The basis for the increased prevalence of GER among the neurologically impaired
population is multifactorial. Muscle spasticity, maintenance in a recumbent position,
malnutrition, altered feeding patterns (especially using nasogastric or gastrostomy tubes),
administration of anticonvulsants and other medications, the presence of kyphoscoliosis, poor
oromotor function, and the use of corrective braces all contribute to GER.
Treatment of GER in the neurologically impaired population is similar to that used in
the neurologically intact population. Acid control is achieved through the use of antacid
therapy, histamine2-receptor antagonists, or proton pump inhibitors. Prokinetic therapy with
metoclopramide has limited utility because the incidence of sedation or irritability is quite
high in this population. Most neurologically impaired children who have GER require
antireflux surgery (variations on Nissen fundoplication) to control the condition, but the rates
of postoperative complications and surgical failure are higher in this population. A
laparoscopic approach to fundoplication may reduce the rate of complication, postoperative
pain, and length of hospital stay. Some controversy surrounds the use of an antireflux
procedure in children who require a gastrostomy tube for nutritional support. Because
clinically significant GER develops in up to 40% of neurologically compromised children
who undergo surgical gastrostomy, many surgeons advocate performing simultaneous
surgical antireflux procedure and gastrostomy. However, recent data suggest that GER can be
managed pharmacologically after surgical gastrostomy in approximately 50% of patients.
Those who subsequently require an antireflux procedure appear to have a similar outcome to
those in whom both procedures are performed simultaneously.
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Unlike the boy described in the vignette, most individuals who have reactive airway
disease associated with environmental allergies have a family history of asthma. Although
pneumonia may occur in this population, malnutrition is uncommon. Immotile cilia syndrome
results in chronic upper and lower respiratory tract disease due to the lack of ciliary clearance
of fluid and foreign material from the upper (sinus and ears) and lower respiratory tracts,
ending in bronchiectasis. Interstitial pneumonitis refers to a group of idiopathic disorders that
result in interstitial or alveolar lung disease. They present with dyspnea, exercise intolerance,
cough, and infiltrates on chest radiography. Some patients respond to corticosteroids or
immunosuppressive therapy. Profound neurologic impairment is not associated with
disorders of mucociliary clearance or interstitial pneumonitis.
References:
Byrne WJ, Euler AR, Ashcraft E, Nash DG, Seibert JJ, Golladay ES. Gastroesophageal reflux
in the severely retarded who vomit: criteria for and results of surgical intervention in
twenty-two patients. Surgery. 1982;91:95-98
Fonkalsrud EW, Ament ME. Gastroesophageal reflux in children. Curr Probl Surg.
1996;33:1-70
Glassman MS, George D, Grill B. Gastroesophageal reflux in children. Clinical
manifestations, diagnosis, and therapy. Gastroenterol Clin North Am. 1995;24:71-98
Lloyd DM, Robertson GS, Johnstone JM. Laparoscopic Nissen fundoplication in children.
Surg Endosc. 1995;9:781-785
Wilkinson JD, Dudgeon DL, Sondheimer JM. A comparison of medical and surgical
treatment of gastroesophageal reflux in severely retarded children. J Pediatr.
1981;99:202-205

2001 Self-Assessment Exercise —

II. Nutrition and nutritional disorders
[Return to Category List]

Questions [Print Directions](1)

Question 8. Answer.
You are discussing with a medical student the optimal nutrient composition of a preterm
infant formula.
Of the following, the MOST accurate statement about such a formula is that
A. casein is the predominant protein
B. copper is the predominant trace mineral
C. lactose is the predominant carbohydrate
D. medium-chain triglyceride is the predominant fat
E. the calcium:phosphorus ratio is 1:1
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Question 28. Answer.
You are writing orders for parenteral nutrition for a 24-hour-old infant who weighs 900 g.
The infant is on a ventilator, but clinically stable.
Of the following, the MOST appropriate order is to
A. add cysteine
B. add sodium to provide 3.0 mEq/kg per day
C. provide a protein intake of 3.0 g/kg per day
D. provide nonprotein calories of at least 30 kcal/kg per day
E. use casein hydrolysate as a source of protein

Question 48. Answer.

The decreased incidence of enteric infections noted in breastfed infants compared with
formula-fed infants is MOST likely due to the
A. more alkaline stool pH in breastfed infants
B. nutritional benefits of human milk on the infant's immune system
C. predominance of Bacteroides and Clostridium in the gut of breastfed infants
D. presence of protective antibodies against enteric infection in human milk
E. sterility of human milk

Question 68. Answer.

A previously healthy 5-day-old male who was born at home develops bruising and melena.
The pregnancy, delivery, and postnatal course were unremarkable. The infant is breastfeeding
vigorously every 2 hours. Findings on physical examination are unremarkable except for
several large bruises. Laboratory testing reveals: hemoglobin, 81 g/L (8.1 g/dL); white blood
cell count, 9.4 x 109/L (9,400/mm3); prothrombin time, 37 seconds; partial thromboplastin
time, 98 seconds; platelet count, 242 x 109/L (242,000/mm3); and fibrinogen, 2.34 g/L (234
mg/dL).
Of the following, the MOST likely cause of the bleeding is
A. disseminated intravascular coagulation
B. factor VIII deficiency hemophilia
C. liver disease
D. vitamin K deficiency
E. von Willebrand disease

Question 90. Answer.

A vaginal wet mount preparation from an 18-year-old girl documents Trichomonas vaginalis.
She is breastfeeding her 2-month-old son exclusively and wishes to do so until he is 6 months
of age.

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Of the following, the BEST treatment for vaginal trichomoniasis in a breastfeeding woman is
A. clindamycin 300 mg orally for 7 days, while continuing to breastfeed
B. clindamycin cream 2% intravaginally at bedtime for 7 days, while continuing to
breastfeed
C. metronidazole 500 mg orally twice a day for 7 days, while continuing to breastfeed
D. metronidazole 2 g orally in a single dose, while ceasing to breastfeed for 24 hours
E. metronidazole gel intravaginally for 5 days, while continuing to breastfeed

Question 108. Answer.

You are starting a preterm infant on parenteral nutrition.
After the minimal nutritional requirements of the healthy infant are met, the aspect of
parenteral nutrition that needs to be adjusted MOST often to reflect the infant's changing
needs is
A. carbohydrate concentration
B. electrolyte concentration
C. intralipid administration
D. total daily protein intake
E. trace mineral content

Question 130. Answer.

A preterm infant receives a formula that is high in polyunsaturated fatty acids.
Of the following, the nutrient that is MOST appropriate to add to the formula to prevent
hemolysis is
A. chromium
B. folic acid
C. selenium
D. vitamin C
E. vitamin E

Question 151. Answer.

Compared with human milk, cow milk formula is MORE likely to contain a(n)
A. greater concentration of essential fatty acids
B. higher protein concentration
C. increased lactose content
D. lower calcium-phosphorus ratio
E. lower iron concentration

Question 169. Answer.

A 2-year-old infant is admitted to the hospital for evaluation of poor weight gain and severe
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diarrhea. Aggressive nutritional rehabilitation is recommended.
Of the following, the PRIMARY advantage of continuous nasogastric feeding over peripheral
parenteral therapy in this situation is
A. controlled achievement of required calories
B. decreased incidence of diarrhea
C. inhibition of pancreatic and biliary secretion
D. provision of trace minerals
E. trophic effects upon gastrointestinal healing

Question 191. Answer.

You have been asked to evaluate a 10-year-old boy who has cirrhosis due to chronic
hepatitis. He is eating a regular diet for age, and you are concerned that this diet may be
inadequate.
Of the following dietary changes, you are MOST likely to recommend a(n)
A. decreased intake of carbohydrate to prevent hyperglycemia
B. decreased intake of minerals to ensure calcium balance
C. decreased intake of protein to prevent encephalopathy
D. increased intake of long-chain fatty acids to compensate for fat malabsorption
E. increased intake of vitamin E to prevent peripheral neuropathy

Question 211. Answer.

A 6-month-old infant is brought to your office for evaluation of diarrhea. At 2 months of age,
she was started on fresh goat milk after she developed vomiting and diarrhea. Physical
examination reveals pallor, poor weight gain, and stomatitis. A complete blood count
documents megaloblastic anemia.
Of the following, the MOST likely etiology of this infant's findings is
A. essential fatty acid deficiency
B. folic acid deficiency
C. protein-losing enteropathy
D. vitamin B12 deficiency
E. vitamin C deficiency

Question 235. Answer.

The mother of a 6-month-old infant does not want to feed her son commercially prepared
baby foods.
Of the following, your BEST advice to the mother is to avoid feeding the infant
A. apple juice
B. corn syrup
C. honey
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D. oatmeal
E. squash

Question 253. Answer.

A mother wishes to breastfeed her infant. She wants to know what she can do to help prevent
dental caries from developing in her child.
Of the following, the MOST effective approach to prevention is to
A. administer 400 U vitamin D daily while breastfeeding
B. avoid introducing juices until after 6 months of age
C. avoid nursing on demand after 1 year of age
D. begin daily fluoride supplementation within the first week of life
E. breastfeed exclusively for the first year of life

Answers

Critique 8. Preferred Response: D

[View Question]
Medium-chain triglycerides (MCTs) are the predominant fats in preterm infant formula. The
intestinal digestion and absorption of fat in preterm infants is limited because of low
intraluminal concentrations of lipases and bile salts. In contrast to long-chain triglycerides,
MCTs, which have chain lengths of 6 to 12 carbons, are hydrolyzed more readily in the
intestine and can be absorbed without lipases or bile salts. After absorption, MCTs do not
have to be re-esterified into triglycerides and transported as chylomicrons; they are
transported directly to the liver via the portal vein as nonesterified fatty acids. In addition,
MCTs can enter mitochondria and be oxidized without carnitine-mediated transport through
mitochondrial membranes. These potential advantages provide the basis for incorporating
MCTs as the principal source of fat in formulas designed for preterm infants.
Calcium is the most abundant mineral in the body and, together with phosphorus,
forms the major inorganic constituent of bone. Mineral retention in the bone is influenced by
the content of calcium and phosphorus in the diet as well as by the dietary
calcium:phosphorus ratio. A preterm infant who receives a dietary intake of calcium of
approximately 250 mg/kg per day from a formula that has a calcium:phosphorus ratio of
approximately 3.8:1 can achieve a mineral retention rate that is similar to the intrauterine
accretion rate of these minerals. The calcium:phosphorus ratio in a preterm infant formula,
therefore, is at least 2:1.
Most preterm infants have a developmental deficiency of lactase, but an abundance of
alpha-glucosidases (sucrase, isomaltase, maltase, glucoamylase) in the small intestine. This
pattern of digestive enzymes is one reason why the carbohydrate in a preterm infant formula
typically includes corn syrup solids (glucose polymers), which partly replace lactose.
Short-chain glucose polymers of 3 to 8 units in length are digested by glucoamylase and
absorbed readily in the gut. Glucose polymers also may enhance gastric emptying and
increase caloric density of the formula without a corresponding increase in osmolality.
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Essential trace minerals in human nutrition include zinc, copper, selenium, chromium,
manganese, molybdenum, and iodine. Among these, the trace mineral with the highest
concentration in a preterm infant formula is zinc. The content of zinc is more than 10-fold
higher than that of copper.
The protein composition of an infant formula needs to be modified for infants of
different gestational ages. An infant formula used for feeding preterm newborns should be
rich in whey protein (lactalbumin) relative to casein and have a whey protein:casein ratio of
60:40, similar to that of human milk. In contrast, an infant formula used for feeding term
newborns may be rich in casein and have a whey protein:casein ratio of 18:82. Whey protein
contains more cystine and less methionine than does casein and is more suitable for a preterm
infant, who may have a limited ability to convert methionine to cystine because of reduced
concentrations of hepatic cystathionase.
References:
Denne SC, Clark SE, Poindexter BR, et al. Nutrition and metabolism in the high-risk
neonate. In: Fanaroff AA, Martin RJ, eds. Neonatal-Perinatal Medicine: Diseases of the
Fetus and Infant. 6th ed. St Louis, Mo: Mosby-Year Book, Inc; 1997:562-621
Reifen RM, Zlotkin S. Microminerals. In: Tsang RC, Lucas A, Uauy R, Zlotkin S, eds.
Nutritional Needs of the Preterm Infant: Scientific Basis and Practical Guidelines.
Baltimore, Md: Williams & Wilkins; 1998:195-207
Woo WWK, Tsang RC. Calcium, magnesium, phosphorus, and vitamin D. In: Tsang RC,
Lucas A, Uauy R, Zlotkin S, eds. Nutritional Needs of the Preterm Infant: Scientific Basis
and Practical Guidelines. Baltimore, Md: Williams & Wilkins; 1998:135-155

Critique 28. Preferred Response: D

[View Question]
The early goal of parenteral nutrition in a very low-birthweight (VLBW) neonate is to
prevent a negative nitrogen balance, which can be accomplished by use of either glucose or
lipid as the nonprotein energy source. A nonprotein energy intake of at least 30 kcal/kg per
day is required in the initial stages of parenteral nutrition to prevent a negative nitrogen
balance. In the later stages, a nonprotein energy intake of at least 70 kcal/kg per day is
required to promote a positive nitrogen balance.
Hepatic activity of cystathionase, which is required for endogenous conversion of
methionine to cysteine, is absent or low throughout gestation and for some time postnatally.
Accordingly, cysteine is an essential amino acid for the newborn. However, it is unstable in
aqueous solution and, therefore, no currently available solution of amino acids for parenteral
use contains cysteine. Cysteine hydrochloride, which is soluble and stable in aqueous
solution, is added as a supplement to the parenteral infusate, but it has a propensity to induce
severe metabolic acidosis. Therefore, it is best to avoid cysteine in a VLBW neonate, who is
susceptible to acid-base imbalance in the early stages of transition from intrauterine to
extrauterine life. Cysteine can be added in the later stages of parenteral nutrition when the
infant can maintain a normal acid-base balance with postnatal maturation.
The evaporative loss of water from skin and the respiratory tract (insensible water
loss) is excessive in a VLBW neonate compared with a term infant, particularly in early
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postnatal life. This higher insensible water loss is attributed to at least three physiologic
factors: greater water permeability of the immature, nonkeratinized skin; higher skin surface
area relative to body weight; and high skin vascularity. Environmental factors such as
phototherapy and respiratory factors such as increased minute ventilation further contribute
to insensible water loss. A VLBW neonate, therefore, is susceptible to hypernatremic
dehydration and its associated complications. As a result, sodium should be added to the
intravenous fluids only after the first week when the infant can maintain a normal
water-electrolyte balance. The sodium requirement of a VLBW neonate is estimated to be 3
to 6 mEq/kg per day.
The protein requirement of a newborn is estimated to be 3.5 to 4.0 g/kg per day. This
intake results in rates of weight gain and nitrogen accretion well in excess of intrauterine
rates and promotes acceptable plasma concentrations of albumin and transthyretin
(prealbumin). However, early introduction and rapid advancement of protein intake is likely
to result in azotemia and hyperaminoacidemia, particularly in unstable infants.
Casein hydrolysate no longer is used as a source of protein in the parenteral nutrition
of newborns; it has been replaced by amino acid solutions. The composition of amino acids
in these solutions is modeled after the serum aminogram pattern of breastfed infants. These
solutions are considered beneficial for weight gain, nutrient retention, and normalization of
plasma concentrations of amino acids.
References:
Denne SC, Clark SE, Poindexter BR, et al. Nutrition and metabolism in the high-risk
neonate. In: Fanaroff AA, Martin RJ, eds. Neonatal-Perinatal Medicine: Diseases of the
Fetus and Infant. 6th ed. St. Louis, Mo: Mosby-Year Book, Inc; 1997:562-621
Heird WC, Gomez MR. Parenteral nutrition. In: Tsang RC, Lucas A, Uauy R, Zlotkin S, eds.
Nutritional Needs of the Preterm Infant: Scientific Basis and Practical Guidelines.
Baltimore, Md: Williams & Wilkins; 1993:225-242
Heird WC, Kashyap S. Protein and amino acid requirements. In: Polin RA, Fox WW, eds.
Fetal and Neonatal Physiology. 2nd ed. Philadelphia, Pa: WB Saunders Co; 1998:654-665
Micheli J-L, Schutz Y. Protein. In: Tsang RC, Lucas A, Uauy R, Zlotkin S, eds. Nutritional
Needs of the Preterm Infant: Scientific Basis and Practical Guidelines. Baltimore, Md:
Williams & Wilkins; 1993:29-46
Pereira GR. Nutritional care of the extremely premature infant. Clin Perinatol.
1995;22:61-75

Critique 48. Preferred Response: D

[View Question]
An increasing body of information confirms that breastfeeding confers protection against
gastrointestinal and respiratory illnesses as well as allergic reactions. These immunologic
advantages are afforded predominantly by the host resistance factors present in human milk
and may be compromised by the addition of other foods to the diet, such as formula or solid
foods. Maternal exposure to foreign antigens stimulates antibody production at the mucosal
surfaces, including the mammary gland. These antibodies, which are present in human milk,
then passively immunize the infant and may contribute to the host defenses of the infant. This
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concept is known as the enteromammary immune system.
Specific factors have been identified in human milk that contribute to its
immunogenicity. A Lactobacillus bifidus growth factor interferes with intestinal colonization
by enteric pathogens. Lactobacilli and bifidobacteria are the predominant organisms isolated
from the colons of breastfed infants compared with Enterobacteriaceae, which are isolated
most often in the stools of formula-fed infants. The presence of Enterobacteriaceae can delay
colonic colonization by normal anaerobic bacteria and may be responsible for the emergence
of nosocomial pathogens. Iron in infant formulas also may contribute to this phenomenon.
Human milk contains lactoferrin, which chelates iron, thus depriving gut bacteria of the
mineral, which is a growth cofactor. Lactoferrin also promotes the growth of lactobacilli and
bifidobacteria.
Additional immunogenic factors that have been isolated from human milk include an
antistaphylococcal factor, secretory immunoglobulin A, complement 3 and 4, lysozyme,
lactoperoxidase, and other immunoglobulins that protect mucosal surfaces. B and T
lymphocytes, neutrophils, and macrophages make up the cellular components of human milk.
Interferon in human milk provides additional protection against infection. The antibacterial
effects also are derived from antibodies to enteric bacteria and viruses that are present in
human milk. Thus, human milk provides both active and passive protection to the newborn.
Using standard preparation techniques that are recommended in the United States, the
microbiologic safety of formula feedings is considered equivalent to that of breastfeeding.
The pH of the stool of a breastfed infant is lower (more acidic) than that of a formula-fed
infant. The acid pH results from the presence of acetate, which is the predominant fatty acid
in the stools of breastfed infants. Propionic and butyric acids are the predominant fatty acids
in the stools of formula-fed infants. Stool pH directly affects colonization of the gut by
pathogenic bacteria. Thus, the acid stool pH of breastfed infants helps decrease colonization
by pathogenic bacteria.
Although human milk is considered the optimal nutrition source for infants,
nutritional factors do not influence the immunologic advantages of this form of feeding.
Rather, they affect its digestibility. The presence of Bacteroides and Clostridium sp in the gut
typically is associated with formula feeding and may increase the likelihood of infection in
this population of infants.
References:
Committee on Nutrition. Breastfeeding. In: Pediatric Nutrition Handbook. 4th ed. Elk Grove
Village, Ill: American Academy of Pediatrics; 1998:1-8
Levy J. Immunonutrition: the pediatric experience. Nutrition. 1998;14:641-647
Xanthou M. Immune protection of human milk. Biol Neonate. 1998;74:121-133

Critique 68. Preferred Response: D

[View Question]
Hemorrhagic disease of the newborn, which results from deficiency of vitamin K, most
commonly presents in healthy, term, breastfed infants during the first week of life. Vitamin K
is present only in small amounts in human milk and is essential for the posttranslation
modification of factors II, VII, IX and X that confers hemostatic activity. Inadequate vitamin
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K decreases the coagulant levels of these factors, prolonging both the prothrombin time
(dependent on factors II, VII, and X) and the partial thromboplastin time (dependent on
factors II, IX, and X). However, as described for the infant in the vignette, fibrinogen levels
remain normal because the synthesis of this globulin does not depend on vitamin K.
Thrombocytopenia is not associated with vitamin K deficiency, but anemia may occur as a
result of the coagulopathy and excessive bleeding.
The classic form of hemorrhagic disease of the newborn occurs in healthy, term
infants who are exclusively breastfed and who have not received prophylactic vitamin K at
birth. Administration of a single intramuscular dose of vitamin K is effective in preventing
this disease. Concerns about the possible carcinogenicity of parenteral vitamin K have not
been confirmed. When routine prophylaxis was discontinued in some communities because
of these concerns, severe and life-threatening bleeding occurred. Although the incidence of
hemorrhagic disease of the newborn is low, the potential for gastrointestinal and even
intracranial hemorrhage warrants continued routine administration of vitamin K.
Early vitamin K deficiency is the rarest form of hemorrhagic disease of the newborn.
It occurs in the first 24 hours of life and is linked to maternal use of medications that interfere
with vitamin K stores or function. Warfarin, anticonvulsants, rifampin, and isoniazid all have
been implicated. The late form of vitamin K deficiency occurs between 2 and 8 weeks of life
and is linked to disorders that compromise the supply of the vitamin. Serious bleeding is most
frequent in this form. Risk factors include breastfeeding, failure to receive vitamin K at birth,
and malabsorption.
All forms of vitamin K deficiency should be treated with slow intravenous or
subcutaneous administration of vitamin K; the intramuscular route should be avoided in the
presence of a coagulopathy. Infants who have serious bleeding should receive fresh frozen
plasma to increase the level of deficient factors rapidly.
Liver disease also is associated with decreases in vitamin K-dependent factors. In
addition, there are decreases in all other coagulation factors except factor VIII (which is not
synthesized in the liver) and other evidence of hepatic dysfunction (eg, hyperbilirubinemia).
Disseminated intravascular coagulation also presents with prolongation of the prothrombin
and the partial thromboplastin times, but affected infants usually appear very ill and have
thrombocytopenia and hypofibrinogenemia. Hemophilia, whether due to factor VIII
deficiency or factor IX deficiency, is associated with prolonged partial thromboplastin time,
but not with prolonged prothrombin time (Figure 68A), thrombocytopenia, or
hypofibrinogenemia.
von Willebrand disease rarely presents in the neonate. Its deficiency of factor VIII is
associated only with prolongation of the partial thromboplastin time.
References:
Andrew M. Developmental hemostasis: relevance to newborns and infants. In: Nathan DG,
Orkin SH, eds. Nathan and Oski's Hematology of Infancy and Childhood. 5th ed.
Philadelphia, Pa: WB Saunders Co; 1998:114-158
Milburn WH. Vitamin K deficiency in breast-fed infants. Pediatr Rev. 1991;12:303

Critique 90. Preferred Response: D

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[View Question]
The protozoan Trichomonas vaginalis causes a characteristic diffuse, yellow-green,
malodorous vaginal discharge (Figure 90A) in most infected women; men usually are
asymptomatic. The only effective antimicrobial agent for the treatment of trichomoniasis is
systemic metronidazole. The treatment regimen of choice is 2 g orally in a single dose, with
500 mg twice a day for 7 days as an alternative regimen. Because metronidazole may have
possible mutagenic effects in infants, it is recommended that lactating women who have
trichomoniasis interrupt breastfeeding for 24 hours after receiving single-dose therapy.
Women using the 7-day regimen should interrupt breastfeeding for the duration of treatment.
Topical metronidazole, topical clindamycin, and systemic clindamycin are effective
treatments for bacterial vaginosis, but they have not been successful in the treatment of
vaginal trichomoniasis.
The list of drugs that are contraindicated in breastfeeding women is relatively small
and can be found in most texts and pediatric reference books. The most up-to-date
information is available at the American Academy of Pediatrics web site
(http://www.aap.org).
References:
Alexander DC. Special drug topics. In: Siberry GK, Iannone R, eds. The Harriet Lane
Handbook. 15th ed. St Louis, Mo: Mosby Year-Book, Inc; 2000:913-914
American Academy of Pediatrics. Antimicrobial agents in maternal milk. In: Pickering LK,
ed. 2000 Red Book: Report of the Committee on Infectious Diseases. 25th ed. Elk Grove
Village, Ill: American Academy of Pediatrics; 2000:103-104
American Academy of Pediatrics. Trichomonas vaginalis infections. In: Pickering LK, ed.
2000 Red Book: Report of the Committee on Infectious Diseases. 25th ed. Elk Grove Village,
Ill: American Academy of Pediatrics; 2000:588-589
Centers for Disease Control and Prevention. 1998 guidelines for treatment of sexually
transmitted diseases. MMWR Morb Mortal Wkly Rep. 1998;47(RR-1):74-75

Critique 108. Preferred Response: B

[View Question]
Parenteral nutrition (PN) is becoming standard therapy for the preterm infant in whom
dextrose solutions alone cannot meet energy and protein requirements. PN is comprised of
carbohydrate (dextrose), protein, fat, vitamins, minerals, and trace minerals. Dextrose is
provided at 4 to 6 mg/kg per minute and is advanced as tolerated to a maximum of
approximately 12.5 g/kg per day. Extremely preterm infants may develop carbohydrate
intolerance because of hypoinsulinemia and poor peripheral glucose utilization. The addition
of insulin to the PN solution will enhance the glucose tolerance of these infants. However,
most preterm infants tolerate increasing dextrose loads without developing hyperglycemia
and glycosuria.
Protein in the form of amino acids should be added as soon as possible in an attempt
to promote positive nitrogen balance. After introducing protein at 1 g/kg per day, increasing
the administration to deliver 2.7 to 3.5 g/kg per day of amino acids will meet the needs of
most preterm infants. The use of newer amino acid mixtures results in a plasma amino acid
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profile similar to that found in healthy breastfed infants. These solutions may decrease the
incidence of PN-associated hepatic dysfunction.
Intravenous fats are a low-volume source of calories and produce less stress on the
respiratory function of the neonate by limiting the carbon dioxide production that is noted
with the administration of carbohydrate. Typically, intravenous lipids are started at 1 g/kg per
day and advanced to a maximum of 4 g/kg per day. Hyperbilirubinemia is a contraindication
to the use of these emulsions, which can displace protein-bound bilirubin, thereby increasing
the risk for kernicterus.
Calcium and phosphorus are needed to mineralize bone, and excessive renal losses
are associated with diuretic and corticosteroid use. The insolubility of these minerals
complicates their administration as part of PN. A calcium-to-phosphorus ratio of 1.7:2.0
seems optimal for mineralization. Trace minerals and fat- and water-soluble vitamins are
added routinely to all PN solutions.
When PN is initiated in the preterm infant, the protein, dextrose, and fat are
administered slowly and do not need to be adjusted in the solution. Trace mineral infusions
are standardized; there have been only rare reports of deficiency syndromes and no studies
confirming toxicity.
Preterm infants undergo both a water and sodium diuresis during the first few days of
life, which is followed by a rapid increase in sodium requirements. Renal failure and diuretic
therapy further complicate salt and water administration. Accordingly, urine output and
serum sodium concentration must be monitored carefully and electrolytes in the PN formula
adjusted as necessary.
References:
Brownlee KG, Kelly EJ, Ng PC, Kendall-Smith SC, Dear PR. Early or late parenteral
nutrition for the sick preterm infant? Arch Dis Child. 1993;69:281-283
Kerner JA Jr. Parenteral nutrition. In: Walker WA, Durie PR, Hamilton JR, Walker-Smith
JA, Watkins JB, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis,
Management. 2nd ed. St Louis, Mo: Mosby-Year Book, Inc; 1996:1904-1960
Pereira GR, Glassman M. Parenteral nutrition in the neonate. In: Rombeau JL, Caldwell MD,
eds. Parenteral Nutrition. Philadelphia, Pa: WB Saunders Co; 1986:702-730
Wesley JR. Efficacy and safety of total parenteral nutrition in pediatric patients. Mayo Clin
Proc. 1992;67:671-675

Critique 130. Preferred Response: E

[View Question]
In 1966, Hassan described a syndrome of hemolytic anemia, reticulocytosis, and
thrombocytosis in preterm infants receiving formulas high in polyunsaturated fatty acids
(PUFAs) and low in vitamin E. The increased erythrocyte fragility and deceased cellular
survival were due to damage to the red blood cell membrane from the metabolic products of
lipid peroxidation. PUFAs are present in the lipid layers of cell membranes. The
auto-oxidation of these lipids by iron-containing enzymes damages cell membranes, thereby
increasing the fragility of the cells. Vitamin E is an antioxidant that inactivates peroxides and
protects cellular membranes. Accordingly, vitamin E should be added to formulas that
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contain high levels of PUFAs to prevent hemolysis.
Anemia is exaggerated by the use of formulas that have increasing PUFA content in
conjunction with iron supplementation. Recognition of this phenomenon resulted in a
reduction of PUFA content in infant formulas and an increase in vitamin E content.
Subsequently, the syndrome became a rare occurrence that was associated with
malabsorption syndromes such as cystic fibrosis. Vitamin E deficiency can result in
neurologic changes that are characterized by decreased deep tendon reflexes, wide-based
gait, ocular palsy, and spinocerebellar degeneration.
Chromium and selenium are trace minerals found in a wide variety of foods.
Chromium deficiency, a rare clinical entity, may result in glucose intolerance due to insulin
resistance, altered nitrogen metabolism, increases in serum fatty acid concentrations, and
encephalopathy. Thyroid dysfunction also may be associated with chromium deficiency.
Selenium is an antioxidant. Patients who are deficient in this trace mineral can develop
myositis, cardiomyopathy, and macrocytic anemia and are more susceptible to vitamin E
deficiency.
Folic acid is a water-soluble vitamin that is important in protein metabolism.
Deficiency of folate is one of the most common hypovitaminoses in humans, especially in the
rapidly growing preterm infant. It results in macrocytic anemia, leukopenia, impaired growth,
and diarrhea. Vitamin C, also a water-soluble vitamin, is an important cofactor for many
metabolic reactions, including cholesterol and carnitine metabolism. Deficiency of this
vitamin results in scurvy, poor wound healing, hemorrhagic and hematologic abnormalities,
and impaired collagen synthesis.
References:
Bieri JG, Corash L, Hubbard VS. Medical uses of vitamin E. N Engl J Med.
1983;308:1063-1071
Gross SJ, Gabriel E. Vitamin E status in preterm infants fed human milk or infant formula. J
Pediatr. 1985;106:635-639
Weber P, Bendich A, Machlin LJ. Vitamin E and human health: rationale for determining
recommended intake levels. Nutrition. 1997;13:450-460
Zipursky A. Vitamin E deficiency anemia in newborn infants. Clin Perinatol.
1984;11:393-402

Critique 151. Preferred Response: B

[View Question]
There are important differences in the composition of human milk and formula. Although
human milk has the same caloric density of formula, it contains a lower concentration of
protein. However, the ease of digestibility and the ideal amino acid composition of human
milk promotes adequate nitrogen balance. This, in part, may reflect the differences in the
whey:casein ratio in human milk (18:82) compared with formula (60:40). These differences
also contribute to difficulties in digesting the milk curd seen in formula-fed infants.
The lactose concentration of human milk and infant formula is equivalent, but the fat
content differs. The total fat and saturated fat content of human milk is higher than cow
milk-based formula. The actual fat content of human milk differs with maternal diet and the
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portion of the feeding. The higher content of fat in the hind milk may help to satiate the
infant. The fats of both human milk and formula are principally in the form of triglycerides,
but the concentration of olein, which is more absorbable, is significantly higher in human
milk. It also appears that the concentration of essential fatty acids is greater in human milk
than infant formula.
Calcium, phosphorus, and iron concentrations are significantly lower in human milk
than in formulas. However, the calcium-to-phosphorus ratio in human milk is 2:1 in contrast
to cow milk formulas, which have ratios of 1.5:1. Although there are differences in skeletal
mineralization among young infants who are bottle- or breastfed, these are transient and are
not believed to be detrimental. Furthermore, the iron in human milk is better absorbed and
partially compensates for the deficiency.
Both human milk and formula contain adequate amounts of vitamins A and C and B
complex vitamins to meet the nutritional needs of infants. The concentrations of vitamins K,
E, and D are higher in formula, but these differences appear to be clinically unimportant in
mothers who consume an adequate diet and are exposed to sunlight. The renal solute load
associated with breastfeeding is lower than that seen in formula-fed infants.
In addition to the quantitative differences between these two forms of infant nutrition,
other factors make breastfeeding preferable. Human milk is rich in lipase, which aids in fat
absorption. The presence of growth factors, such as epidermal growth factor, in human milk
has a profound effect on neonatal gut development.
There are also differences in gastrointestinal hormonal responses among breastfed and
formula-fed infants. Serum concentrations of motilin, gastrointestinal polypeptide, insulin,
and pancreatic polypeptide are higher in bottle-fed infants and may be the result of
differences in composition or feeding volume.
References:
Fomon SJ. Nutrition of Normal Infants. Philadelphia, Pa: BC Decker; 1993
George DE, DeFrancesca BA. Human milk in comparison to cow milk. In: Lebenthal E, ed.
Textbook of Gastroenterology and Nutrition in Infancy. 2nd ed. New York, NY: Raven Press;
1989:242-243
Lawrence RA. Breastfeeding: A Guide for the Medical Profession. 4th ed. St Louis, Mo:
Mosby-Year Book, Inc; 1994
LeLeiko NS, Chao C. Nutritional requirements. In: Rudolph AM, Hoffman JIE, Rudolph CD,
eds. Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange; 1996:1001-1010

Critique 169. Preferred Response: E

[View Question]
Enteral alimentation is more physiologic, less costly, and associated with fewer
complications than parenteral nutrition. The selection of a formula for enteral feeding is
based upon the child’s age and gastrointestinal function and the underlying disease.
Contraindications to nasogastric tube feedings include intestinal obstruction, persistent
vomiting, severe respiratory distress, upper gastrointestinal bleeding, and necrotizing
enterocolitis.
The lack of enteral stimulation of the gut seen with parenteral nutrition may result in
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alterations in gut microflora, impaired gut immune function, and disruption of the integrity of
the mucosal barrier. Decreased villous height, cellular mass, and brush border enzymes also
result. Even small volumes of enterally administered nutrition can have a trophic effect on
the small intestine and result in increased mucosal weight and DNA content, increased brush
border enzyme concentrations, and cellular turnover. Children who have protracted diarrhea
and malnutrition can benefit from enteral feedings if the volume and concentration of the
formula are advanced slowly.
Continuous feedings result in fewer stools and improved nutritional rehabilitation.
Mechanisms by which continuous enteral feedings improve the clinical outcome in these
patients include decreased gastrocolic reflex due to reduced gastric distension and decreased
postprandial vomiting and dumping syndrome. In older children who have Crohn disease,
enteral feedings have proven effective in promoting remission and improving nutritional
status and growth. Infants who have short bowel syndrome are started on enteral feedings as
early as possible in an attempt to stimulate gut adaptation and to avoid parenteral
nutrition-associated liver disease. Weight gain and positive nitrogen balance can be achieved
in most of these children. Enteral feedings also have been used in children who have liver
disease and to treat growth failure in infants who have gastroesophageal reflux.
Diarrhea is the most common complication of enteral feedings and occurs in 10% to
30% of patients. Often the diarrhea has a multifactorial etiology and may result from
malabsorption, osmolarity of the formula, or antibiotic use. Recurrent emesis also can occur
in the enterally fed infant. Fluid and electrolyte abnormalities are rare when fluid balance is
assessed carefully. Mechanical complications such as kinking and clogging may be
associated with the use of small-bore feeding tubes. Tube placement must be confirmed to
avoid aspiration and dumping syndrome if the gastric tube advances into the small intestine.
Dumping syndrome is characterized by the development of abdominal distension, diarrhea,
sweating, tachycardia, and hypoglycemia and results from passage of hypertonic or
hyperosmolar fluids into the duodenum.
The incidence of complications with enteral feedings is comparable to that of
parenteral feedings, but the complications are less significant with enteral feedings.
Continuous enteral feedings reduce pancreatic and biliary secretions by avoiding the
meal-related release of enteric hormones. Caloric and trace mineral requirements are
provided effectively by either form of nutrition.
References:
American Society for Parenteral and Enteral Nutrition. Guidelines for the use of parenteral
and enteral nutrition in adult and pediatric patients. JPEN J Parenter Enteral Nutr.
1993;17(suppl 4):1SA-52SA
Heyman MB. Specialized nutritional support-enteral and parenteral nutrition. In: Rudolph
AM, Hoffman JIE, Rudolph CD, eds. Rudolph's Pediatrics. 20th ed. Stamford, Conn:
Appleton & Lange; 1996:1018-1025
Moore FA, Feliciano DV, Andrassy RJ, et al. Early enteral feeding, compared with
parenteral, reduces postoperative septic complications. The results of a meta-analysis. Ann
Surg. 1992;216:172-183
Sutphen JL, Abad-Sinden A. Enteral nutrition. In: Walker WA, Durie PR, Hamilton JR,
Walker-Smith JA, Watkins JB, eds. Pediatric Gastrointestinal Disease: Pathophysiology,
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Diagnosis, Management. 2nd ed. St Louis, Mo: Mosby-Year Book, Inc; 1996:1884-1903

Critique 191. Preferred Response: E

[View Question]
In approximately 50% of children who have cirrhosis, a decrease in delivery of bile acid to
the small intestine results in malabsorption of fat and fat-soluble vitamins. The malabsorption
occurs when the intraluminal concentration of bile acids falls below the level required for
micelle formation, which is necessary for long-chain fatty acid lipolysis and absorption. A
decrease in the bile salt pool also contributes to the fat malabsorption. Medium-chain
triglycerides are more readily absorbed than long-chain fatty acids in the presence of low bile
acid concentrations, in part because they do not require the same degree of lipolysis. Fat
malabsorption results in malnutrition, growth retardation, and steatorrhea. Increased intake of
long-chain fatty acids will exacerbate steatorrhea.
The fat-soluble vitamins A, D, E, and K also require solubilization by bile acids into
micelles for absorption. Deficiency syndromes for each of these vitamins have been
described in children who have chronic liver disease. Vitamin A is required to maintain skin
integrity and cell differentiation. Deficiency can result in dermatologic abnormalities
(xerophthalmia) and night blindness. Vitamin D regulates intestinal calcium and phosphorus
absorption and renal excretion and is required for bone mineralization. Deficiency of this
vitamin causes osteopenia, rickets, and an increase in urinary excretion of amino acids.
Vitamin K is involved in hepatic synthesis of several clotting factors, and a deficiency can
result in clotting abnormalities. Vitamin E is an antioxidant that can protect cell membranes
from polyunsaturated fatty acids. Deficiency of this vitamin is associated with neuromuscular
degeneration that is characterized by areflexia, ataxia, posterior column dysfunction, and
peripheral neuropathy. Anemia and hemolysis also can occur. Supplementation of two to four
times the recommended daily allowance of vitamin E in an aqueous form is recommended.
Glucose intolerance is uncommon among children who have cirrhosis in the absence
of hepatic failure. Excessive intake of protein by children who have cirrhosis can precipitate
hepatic encephalopathy, but the increased requirements for protein synthesis among these
children demands maintenance of an adequate intake. Due to the malabsorption of fats,
dietary calcium often will bind to the intraluminal fats, thereby preventing absorption of this
mineral. Indeed, an increase in calcium may be needed.
References:
Murray KF, Jonas MM. Biliary atresia. In: Altschuler SM, Liacouras CA, eds. Clinical
Pediatric Gastroenterology. Philadelphia, Pa: Churchill Livingstone; 1998:331-340
Nompleggi DJ, Bonkovsky HL. Nutritional supplementation in chronic liver disease: an
analytical review. Hepatology. 1994;19:518-533
Sokol RJ, Heubi JE, Iannaconne ST, Bove KE, Balistreri WF. Vitamin E deficiency with
normal serum vitamin E concentrations in children with chronic cholestasis. N Engl J Med.
1984;310:1209-1212

Critique 211. Preferred Response: B

[View Question]
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In the past, goat milk has been fed to children who have cow milk or soy protein intolerance.
Goat milk is high in essential fatty acids and has a higher content of medium-chain
triglycerides than cow milk. However, it contains lactose as a carbohydrate, making it an
unsuitable alternative for children who are lactose-intolerant. In addition, goat milk has a
high protein content, precluding its use in young infants. Finally, goat milk does not contain
folic acid, making supplementation essential for infants if this is their sole nutritional source.
Goat milk fortified with folic acid is commercially available.
Folic acid is distributed widely in plant and animal tissues and is absorbed rapidly in
the duodenum and jejunum. Its bioavailability ranges from 25% to 95%, depending upon the
food ingested. Green vegetables are good sources. Unlike goat milk, human milk and cow
milk contain modest concentrations of the vitamin. Folic acid is heat-sensitive and is
metabolized by and stored in the liver. Serum levels fall during early infancy, necessitating
supplementation of infant formulas. It is estimated that the liver contains approximately a 3
month reserve of folic acid. Bacteria present in the small intestine of humans also produce
folic acid.
The active form of folic acid is tetrahydrofolic acid (THF), an important cofactor in
nucleotide metabolism and RNA and DNA synthesis. Because THF plays an essential role in
cell replication, a deficiency in this vitamin results in a slowing or arrest of this process. The
effects of THF deficiency are most evident in cells that have the highest rates of replication,
such as the intestinal tract and bone marrow. Because vitamin B12 is an important cofactor in
THF metabolism, its deficiency results in a hematologic picture similar to that seen with folic
acid deficiency. However, neurologic damage also is associated with vitamin B12 deficiency,
and the central nervous system insult may not be reversible with therapy. Megaloblastic
anemia and hypersegmentation of neutrophils are the hematologic alterations associated with
a deficiency of folic acid, one of the most common deficiencies in humans, especially during
periods of rapid growth (eg, infants) or cell turnover (eg, sickle cell anemia, thalassemia,
hemolytic disease, pregnancy). Accordingly, the symptoms described for the infant in the
vignette are most indicative of folic acid deficiency.
Drugs such as phenytoin, sulfasalazine, and oral contraceptives may interfere with
folic acid absorption. Trimethoprim competes for dihydrofolate reductase, the enzyme
responsible for folic acid conversion to THF. Antibiotics also alter the intestinal bacterial
flora and may decrease the amount of folic acid produced in the colon. Folic acid
malabsorption may be associated with diarrhea in infants and alcoholism and cirrhosis in the
adult.
Essential fatty acid deficiency produces a dry and flaky skin, poor hair growth, a
reduced growth rate, thrombocytopenia, and poor wound healing. It is an unusual deficiency
state that is seen in infants being maintained with fat-free total parenteral nutrition.
Protein-losing enteropathy describes a process by which injury to the stomach, small
intestine, or colon results in intestinal protein loss and hypoalbuminemia. Causes during
childhood include inflammatory bowel disease, intestinal lymphangiectasia, gluten
sensitivity, food allergies, and gastrointestinal infections. Abdominal pain, diarrhea, and
edema characterize these disorders. Vitamin C deficiency produces a hemorrhagic tendency
and pain upon movement. It is associated with prolonged use of heated formulas in infants
who are not receiving adequate vitamin C supplementation.

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References:
Greer FR. Nutritional needs of the full-term and low-birthweight infant. In: Rudolph AM,
Hoffman JIE, Rudolph CD, eds. Rudolph's Pediatrics. 20th ed. Norwalk, Conn: Appleton &
Lange; 1996:239-244
McLaren DS. Clinical manifestations of human vitamin and mineral disorders: a resume. In:
Modern Nutrition in Health and Diseases. 8th ed. Philadelphia, Pa: Lea & Febiger;
1994:909-923
Mentzer WC. Megaloblastic anemia. In: Rudolph AM, Hoffman JIE, Rudolph CD, eds.
Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange; 1996:1181-1184

Critique 235. Preferred Response: C

[View Question]
Botulism is an acute paralytic disease caused by a neurotoxin produced by Clostridium
botulinum. The toxin is carried to the peripheral cholinergic synapses where it irreversibly
binds to the synaptic membranes and prevents acetylcholine release. This blockade prevents
autonomic and neuromuscular transmission. Infantile botulism develops after the ingested
spores of clostridia germinate in the colon and subsequently produce the toxin. Both the toxin
and bacteria are found in the stools of affected infants, but the bacteria are not transmitted
from person to person.
Approximately 95% of the cases of infant botulism occur in children between 3 weeks
and 6 months of age, with both genders affected equally. Notably, infants are the only
members of the family who become ill. This form of C botulinum infection is uncommon,
accounting for only about 100 cases annually. Risk factors include the ingestion of honey
(confirmed in 15%) and a decreased number of bowel movements, suggestive of slow
gastrointestinal transit. Accordingly, the mother described in the vignette should avoid
feeding honey to her infant son. Neither light nor dark corn syrup has been identified as a risk
factor for botulism; either may be used safely during infancy. Breastfeeding, perhaps because
of the associated rapid gastrointestinal transit, may be protective against infantile botulism.
The symptoms of botulism in infants begin abruptly and include poor feeding, weak
suck, feeble cry, drooling, and obstructive apnea. Fatigability with repetitive motor activity is
the hallmark of the disease. Lethargy and listlessness often are noted as well. Generalized
weakness and hypotonia are late manifestations and necessitate hospitalization. Constipation
is present in most infants who have botulism, but this symptom often is overlooked. In some
infants, infantile botulism is clinically indistinguishable from sudden infant death syndrome,
of which up to 5% of cases may be due to botulism.
Treatment is supportive, with particular attention to the infant’s respiratory and
nutritional needs. Antibiotic therapy may increase the release of the neurotoxin and should be
avoided if possible. Equine antitoxin rarely is used in infantile botulism because a lifelong
hypersensitivity may develop. Human-derived antitoxin may prove effective in the treatment
of this disorder. Full recovery is expected in the absence of complications, but it may require
several months. The central nervous system is spared because the toxin does not penetrate the
blood-brain barrier. Therefore, intelligence and personality development are not affected.
Apple juice has been associated with the development of diarrhea or constipation in
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infants, but it has not been implicated in C botulinum infection. With proper techniques,
oatmeal and squash can be prepared safely for infant consumption at home.
References:
Johnson RO, Clay SA, Arnon SS. Diagnosis and management of infant botulism. Am J Dis
Child. 1979;133:586-593
Lilly T, Rhodehamel EJ, Kautter DA, Solomon HM. Clostridium botulinum spores in corn
syrup and other syrups. J Food Protect. 1991;54:585-587
Schreiner MS, Field E, Ruddy R. Infant botulism: a review of 12 years' experience at the
Children's Hospital of Philadelphia. Pediatrics. 1991;87:159-165
Spika JS, Shaffer N, Hargrett-Bean N, Collin S, MacDonald KL, Blake PA. Risk factors for
infant botulism in the United States. Am J Dis Child. 1989;143:828-832

Critique 253. Preferred Response: C

[View Question]
Nursing-bottle caries are not found exclusively in formula-fed infants; any child who has
teeth and falls asleep with nutrient materials such as milk or juice in the mouth is at risk for
developing caries of the upper incisors. Breastfed infants who sleep with their mothers and
nurse frequently on demand through the night are as much at risk as infants who are put to
bed with a bottle of milk or juice. Avoiding nursing on demand at night after 1 year of age
will prevent this problem.
Breastfeeding exclusively through the first year of life will not have an adverse
impact on the infant’s teeth unless the infant nurses frequently at night, as described
previously. Delaying the introduction of juice until 6 months of age has little impact on
dental caries because most infants do not acquire their first teeth until 6 to 7 months of age.
The juice is only a problem when it is provided to the infant during the night and the baby
falls asleep with the bottle in his or her mouth.
Although there is very little fluoride in human milk, there is no evidence that
providing fluoride supplementation to breastfed infants in the first 6 months of life prevents
dental caries. After 6 months of age, fluoride supplementation may be given in communities
where the fluoride concentration in the water is less than 0.3 parts per million. Vitamin D
supplementation of exclusively breastfed infants is recommended, but this has no benefit in
preventing dental caries.
References:
Kula KS, Wright JT. Oral problems. In: McMillan JA, DeAngelis CD, Feigin RD, Warshaw
JB, eds. Oski's Pediatrics: Principles and Practice. 3rd ed. Philadelphia, Pa: Lippincott
Williams & Wilkins; 1999:641-660
Shusterman S. Pediatric dental update. Pediatr Rev. 1994;15:311-318

2000 Self-Assessment Exercise —

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[Return to Category List]

Questions [Print Directions](2)

Question 30. Answer.

You note that a previously healthy 15-month-old boy appears pale. He has been fed goat milk
exclusively since birth. Laboratory findings include: hemoglobin, 6.1 g/dL; white blood cell
count, 4,800/mm3; platelets, 144,000/mm3; mean corpuscular volume, 109 fL; and
differential count, 29% neutrophils, 68% lymphocytes, and 3% monocytes. There also is
hypersegmentation of the neutrophils.
Of the following, the MOST likely cause of the hematologic abnormalities is
A. acute lymphoblastic leukemia
B. Fanconi anemia
C. folate deficiency
D. iron deficiency
E. vitamin B12 deficiency

Question 85. Answer.

A 2-year-old boy is brought to your office because of poor growth. His parents comment that
he had been evaluated by an allergist earlier in the year for diarrhea. Skin testing revealed
allergy to milk, wheat, and eggs. With complete dietary restriction of these foods, his
diarrhea resolved.
Of the following, the MOST likely explanation for this child's poor weight gain is
A. allergic reaction to other foods
B. eosinophilic gastroenteritis
C. insufficient caloric intake
D. pancreatic insufficiency
E. undiagnosed celiac disease

Question 166. Answer.

Peripheral alimentation is instituted in a 3-year-old child who has short gut syndrome.
Of the following, the MOST appropriate laboratory study to be monitored within the first 24
hours of therapy is
A. hemoglobin concentration
B. platelet count
C. serum amylase concentration
D. serum electrolyte concentrations
E. white blood cell count
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Question 233. Answer.
You are discussing with a medical student the benefits of breastfeeding in terms of
preventing infectious diseases during infancy.
Of the following pathogens, it is MOST likely that breastfeeding provides protection against
infection caused by
A. cytomegalovirus
B. Escherichia coli
C. herpes simplex virus
D. human immunodeficiency virus
E. Mycobacterium tuberculosis

Answers

Critique 30 Preferred Response: C

[View Question]
Infants fed exclusively goat milk are prone to folate deficiency and as a consequence,
megaloblastic anemia. The megaloblastic anemias are a complex and relatively uncommon
group of disorders. They usually share several features, including macrocytic anemia,
thrombocytopenia, leukopenia, and neutropenia. The peripheral blood smear reveals
hypersegmentation of neutrophils and large ovalocytic erythrocytes. The bone marrow
usually contains giant metamyelocytes and large erythroid precursors in which the nuclear
chromatin has a typical fine, lacy appearance. The common pathogenetic feature of
megaloblastic anemias is that cells synthesize their RNA and cytoplasmic constituents faster
than DNA, resulting in relative immaturity of the nucleus compared with the cytoplasm.
Megaloblastic anemia most commonly is due to the deficiency of either folate or
vitamin B12. Isolated nutritional deficiency of folate is uncommon, but it always should be
considered when an infant has been fed unsupplemented goat milk exclusively. The folate
content of goat milk is approximately 10% that of human or cow milk. Folate deficiency after
infancy usually is compounded by additional factors, such as general malnutrition, unusual
diets, increased folate requirements, folate malabsorption, and drugs that inhibit folate
metabolism. Metabolic defects of folate metabolism are rare.
Vitamin B12 deficiency due purely to dietary deficiency is unusual, even though a
strict vegetarian diet is a poor source of the vitamin. B12 deficiency most often is due to
pernicious anemia, in which an autoimmune process destroys the intrinsic factor-producing
gastric parietal cells. The resulting deficiency of intrinsic factor prevents normal absorption
of vitamin B12. Vitamin B12 deficiency also results from disorders that impair gastric and
small intestinal absorption and, rarely, from inherited metabolic defects.
The critical clinical feature of pernicious anemia is degeneration of the posterior and
lateral columns of the spinal cord as well as a peripheral neuropathy. Loss of vibrational and
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positional sense, ataxia, spasticity, depression, and dementia can occur and may be
irreversible. These complications do not occur in folate deficiency.
The evaluation of megaloblastic anemia is complex and should be undertaken in
consultation with a hematologist. The diagnosis of folate deficiency is based best on a low
concentration of folate in red blood cells and not on the less specific and more variable serum
levels. In all patients in whom folate deficiency is suspected, it is critical to exclude vitamin
B12 deficiency as well because treatment of vitamin B12 deficiency with high doses of folate
may delay the diagnosis of vitamin B12 deficiency. Vitamin B12 is measured in serum, but
patients who have low serum levels of vitamin B12 also may have low levels of folate.
Therefore, it is important to measure concentrations of both vitamins to avoid a misdiagnosis.
Children who have megaloblastic anemia require prompt diagnosis and treatment. Any delay
could result in a worsening of neurologic complications and increase the risk that neurologic
recovery may be incomplete.
Acute lymphoblastic leukemia may present with pancytopenia, but the anemia is
normocytic, and there is no hypersegmentation of the neutrophils. Fanconi anemia presents
with pancytopenia and macrocytosis, but hypersegmentation is not noted, and usually there
are typical congenital malformations. Iron deficiency anemia should result in a hypochromic,
microcytic anemia rather than the macrocytic anemia described in the vignette.
References:
Babior BM. The megaloblastic anemias. In: Beutler E, Lichtman MA, Coller BS, Kipps TJ,
eds. Williams Hematology. 5th ed. New York, NY: McGraw-Hill Information Services, Inc;
1995:471-489
Whitehead VM, Rosenblatt DS, Cooper BA. Megaloblastic anemia. In: Nathan DG, Orkin
SH, eds. Nathan and Oski's Hematology of Infancy and Childhood. 5th ed. Philadelphia, Pa:
WB Saunders Co; 1998:385-422

Critique 85 Preferred Response: C

[View Question]
The gastrointestinal (GI) tract plays a central role in the development of food allergy, serving
both as a target organ for the immunologic reaction and as part of the immunologic
processing of food antigens. Gut-associated lymphoid tissues, predominantly located in the
Peyer patches of the small intestine produce immunoglobulin A (IgA) and lymphocytes.
Antigenic macromolecules are taken up by the GI tract via the enterocyte through
intracellular gaps and by M cells overlying the Peyer patches. Mucosal (eg, glycoprotein) and
luminal (eg, bacterial) factors deter the penetration of these allergenic proteins. Increased
antigen uptake due to local environmental factors, in concert with a genetically
predetermined activation of lymphocytes, is necessary for the development of food allergy.
Adverse reactions to foods are categorized as food intolerance and food allergy. Food
intolerance is defined as the nonimmunologic reaction to a food or its additive (eg, toxin, dye,
contaminant). Food allergy describes immunologically based abnormal reactions to foods.
Food allergy can be of the immediate type (reaginic IgE and mast cell-mediated),
antigen-antibody immune complex type (IgG-mediated or type III reaction), or the delayed or
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T cell-mediated type (type IV reaction).
Reaction to cow milk protein is the most common food allergy during infancy,
affecting 0.2% to 7.5% of all children. Those who have a family history of food allergy are
four to five times more likely to develop an allergic disease. Common food antigens include
egg protein (ovalbumin), soy proteins, beef, pork, fish and shrimp, peanuts and other
legumes, nuts and seeds, wheat and other grains, strawberries, and yeast products. A positive
food challenge remains the hallmark for the diagnosis of gastrointestinal food allergy. In
these instances, single- or double-blind food challenges are recommended. In some cases, the
individual situation often makes such a food challenge unnecessary or ill-advised (eg, history
of anaphylaxis). Skin-prick testing; radioallergosorbent (RAST) or enzyme-linked
immunosorbent assay (ELISA) IgE and IgG testing; and histologic inspection of biopsied
gastric, small intestine, or colonic mucosa also are helpful adjunctive tests to establish the
diagnosis of food allergy.
The primary treatment for a child who has a food allergy is to remove the offending
antigen(s) from the diet. Over time, many children who have food allergy will develop
tolerance to the food, making cautious, periodic attempts to introduce the offending food
possible. An elimination diet often can be successful in children who have single food
allergy. However, dietary modification and nutritional counseling may be necessary for
children who have multiple food allergies to identify hidden ingredients in processed foods
and cross-reacting foods (eg, peanuts, legumes). Aggressive restriction of allergenic foods
may compromise the nutritional adequacy of the diet and interfere with the normal growth of
the child. This is the most likely explanation for the poor weight gain in the child described
in the vignette. In children who have multiple allergies, medical therapy with disodium
cromoglycate and oral ketotifen have been found to be effective. However, their use should
be restricted to patients in whom dietary control of the food allergy cannot be achieved.
Immunotherapy by injection or sublingual administration of offending antigens has not
proven to be effective in the management of patients who have food allergy.
Prevention of food allergy in the infant at high risk (eg, a family history of atopy or
food allergy or an elevated cord blood IgE) can reduce the incidence of allergy in this
population. Exclusive breastfeeding for 4 to 6 months by mothers who are following a diet in
which milk, beef, eggs, and fish consumption are restricted or infant feeding with a
hydrolysate formula is recommended. Delayed introduction of solid foods after 6 months and
avoidance of milk and egg products beyond 12 months of age is advocated.
Pancreatic insufficiency is not a manifestation of food intolerance. The improvement
of the diarrhea described in the vignette following the exclusion of only milk, wheat, and
eggs is not consistent with celiac disease. The pathophysiology underlying celiac disease is
an inflammatory reaction triggered by the gliadin fraction of gluten. Dietary restriction must
exclude all foods that contain gluten, including wheat, rye, oats, malt, and barley. Such a
restriction results in catch-up growth or resumption of a normal rate of growth. Similarly,
eosinophilic gastroenteritis rarely responds to dietary modification alone; pharmacologic
therapy frequently is needed to reverse the associated diarrhea and growth delay.
References:
Bock SA, Sampson HA. Food allergy in infancy. Pediatr Clin North Am. 1994;41:1047-1067
Jewett DL, Fein G, Greenberg MH. A double-blind study of symptom provocation to
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determine food sensitivity. N Engl J Med. 1990;323:429-433
Kerner JA Jr. Formula allergy and intolerance. Gastroenterol Clin North Am. 1995;24:1-25

Critique 166 Preferred Response: D

[View Question]
Peripheral alimentation typically is administered to patients in whom nutrition support is
expected to be limited to 7 to 10 days. Because of its short duration; limits on the
carbohydrate, fat, and calcium concentrations; and the relatively slow rate of administration,
this nutrition therapy is relatively free of complications. However, most patients receiving
peripheral alimentation have previous and ongoing gastrointestinal electrolyte losses that
may result in a metabolic deficit. Therefore, it is essential to provide an alimentation solution
that meets the patient's metabolic and fluid requirements. Serum electrolyte concentrations
would be subject to the most acute variations if the patient's requirements are not being met
and, therefore, should be monitored carefully within the first 24 hours of therapy.
Thrombocytopenia also can occur in patients receiving parenteral alimentation,
although it is an uncommon early complication and has been associated with the
administration of intravenous fat or deficiencies in trace elements. Pancreatitis is an
uncommon complication of peripheral alimentation, so determination of serum amylase
concentrations is recommended only in those patients who report abdominal pain. The white
blood cell count can be a useful monitor for catheter-related sepsis, but it is obtained
routinely only on a weekly basis in patients receiving prolonged parenteral alimentation.
Complications occurring in patients receiving central parenteral nutrition can be
divided into three categories: mechanical, infectious, and metabolic. The predominant
complication associated with parenteral nutrition is catheter-related infection, which often is
the result of improper care of the catheter. Frequent dressing changes using sterile technique
are essential to prevent such infections. Staphylococcus epidermidis is the pathogen isolated
most frequently. Initial antibiotic therapy through the catheter should be guided by the
bacterial sensitivities documented in the community, but treatment generally includes
vancomycin, gentamicin, or both. Most patients can be cured without removing the infected
catheter if appropriate antibiotic therapy is continued for 14 to 21 days. In patients who
remain febrile or who have a positive blood culture after 2 to 4 days of antibiotic therapy, the
catheter should be removed.
Mechanical complications occur almost exclusively in patients receiving alimentation
via the central venous route and may develop when inserting the catheter or during prolonged
use. Complications that may occur at the time of catheter insertion include pneumothorax,
hematoma or laceration of the subclavian vein, air embolism, catheter malposition, cardiac
perforation, injury to the phrenic nerve, and hemothorax. A catheter that is in place can be
dislodged, with resultant fluid leaks into the pericardial, pleural, and mediastinal spaces.
Venous thrombosis that causes superior vena cava syndrome and pulmonary embolus also
may occur during hyperalimination.
Fluid electrolyte, vitamin, mineral, and trace element abnormalities occur when the
patient's needs either are not met or are exceeded. Hyperglycemia resulting in glycosuria and
osmotic diuresis occurs when the rate of carbohydrate infusion exceeds the patient's
utilization rate or when the patient becomes insulin-resistant as a result of sepsis,
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corticosteroid use, or surgical stress. Excessive administration of carbohydrates can cause
pulmonary failure.
Hepatic dysfunction, including hepatomegaly, cholestasis, fatty infiltration of the
liver, fibrosis and cirrhosis, and cholelithiasis are associated with prolonged administration of
parenteral alimentation, low birthweight, prematurity, gastrointestinal surgery, sepsis, and the
absence of oral intake.
The key to safe administration of parenteral nutrition is close monitoring so that
problems are detected early and appropriate changes are made in the infusate. Daily
assessments of weight and vital signs, strict maintenance of intake and output, and
monitoring of blood and urine tests are essential. Baseline studies include a complete blood
count, serum electrolytes, triglycerides, cholesterol, total protein and albumin, trace minerals,
liver alanine aminotransferase, gamma-glutamyl transpeptidase, alkaline phosphatase, and
renal function tests. After the adequacy of the alimentation solution is established, ongoing
monitoring is needed. Weekly measurement of glucose, renal and liver function, bilirubin,
magnesium, electrolytes, minerals, triglycerides, cholesterol, and a complete blood count are
recommended. Levels of iron, vitamins, and trace elements and anthropometric
measurements should be assessed at least monthly.
References:
Greene HL, Hambidge KM, Schanler R, Tsang RC. Guidelines for the use of vitamins, trace
elements, calcium, magnesium, and phosphorus in infants and children receiving total
parental nutrition: report of the Subcommittee on Pediatric Parenteral Nutrient Requirements
from the Committee on Clinical Practice Issues of the American Society for Clinical
Nutrition. Am J Clin Nutr. 1988;48:1324-1342
Heird WC. Parenteral nutrition. In: Grand RJ, Sutphen JL, Dietz WH, eds. Pediatric
Nutrition: Theory and Practice. Boston, Mass: Butterworths Publishers; 1987:747-761
Kerner JA Jr. Parenteral nutrition. In: Walker WA, Durie PR, Hamilton JR, Walker-Smith
JA, Watkins JB, eds. Pediatric Gastrointestinal Disease: Pathophysiology, Diagnosis,
Management. 2nd ed. St Louis, Mo: Mosby-Year Book, Inc; 1996:1904-1951

Critique 233 Preferred Response: B

[View Question]
Human milk is protective against enteropathogenic Escherichia coli and other
gastrointestinal pathogens. This protection is greatest during an infant's first 3 months of life
and declines with increasing age. During the weaning period, partial breastfeeding continues
to confer some protection. The mechanisms of protection are at least threefold. Breastfeeding
confers protection through active components of human milk, which include cells, antibodies,
carrier proteins, enzymes, and hormones. The process of breastfeeding itself may decrease
exposure to enteropathogenic E coli that could be present in contaminated bottles, milk, or
water. Finally, administration of human milk initiates and maintains the growth of
Lactobacillus bifidus in the gut; this decreases luminal pH, which inhibits the growth of E
coli. For these and other reasons, breastfeeding should be encouraged.
Breastfeeding is contraindicated in women who have human immunodeficiency virus
(HIV) infection because human milk is a well-known source of transmission of this virus.
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HIV virions have been observed by electron microscopy within histiocytes and in the
cell-free fraction of human milk. Colostrum contains a higher concentration of lymphocytes
and macrophages than mature milk and, therefore, is more likely to harbor cell-associated
viruses such as HIV. The risk of transmission of HIV through breastfeeding is increased
when infection is recent or illness is more advanced in the mother. Both of these clinical
situations are associated with a high viral load in body fluids, including human milk.
Human milk does not confer protection against herpes simplex virus (HSV). Perinatal
HSV infection can occur by transplacental, intrapartum, or postnatal transmission. The latter
is most likely to occur following contact with orolabial herpes. Postnatal transmission of
HSV also can occur if breast lesions are present.
Human milk does not confer protection against Mycobacterium tuberculosis.
Neonatal tuberculosis is acquired in four ways: by inhalation of infected droplets (via the
lung), by ingestion of infected droplets (via the gut), by contamination of traumatized skin or
mucous membranes, or by ingestion of infected milk. Among these routes of acquisition, the
lung is by far the most common portal of entry in the neonate.
Human milk also is a source of transmission of cytomegalovirus (CMV). CMV
infection is an endemic, often subclinical infection among women of low socioeconomic
status. Prolonged viral shedding of CMV is common, primarily through the genital tract and
milk. The fetus can be infected by the transplacental route. However, the newborn is infected
more frequently by contamination from the genital tract during birth or by ingestion of
infected milk.
References:
Kohl S. Neonatal herpes simplex virus infection. Clin Perinatol. 1997;24:129-150
Nelson CT, Demmler GJ. Cytomegalovirus infection in the pregnant mother, fetus, and
newborn infant. Clin Perinatol. 1997;24:151-160
Ogra PL, Rassin DK. Human breast milk. In: Remington JS, Klein JO, eds. Infectious
Diseases of the Fetus & Newborn Infant. 4th ed. Philadelphia, Pa: WB Saunders Co;
1995:108-139
Ruff AJ. Breastmilk, breastfeeding, and transmission of viruses to the neonate. Semin
Perinatol. 1994;18:510-516
Smith MHD, Teele DW. Tuberculosis. In: Remington JS, Klein JO, eds. Infectious Diseases
of the Fetus & Newborn Infant. 4th ed. Philadelphia, Pa: WB Saunders Co; 1995:1074-1086

1999 Self-Assessment Exercise —

II. Nutrition and nutritional disorders
[Return to Category List]

Questions [Print Directions](3)

Question 7. Answer.
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A 12-year-old girl complains of severe headache and pain in her arms and legs. The onset of
symptoms has been gradual, but the leg pain has intensified such that she cannot bear weight
on her right leg. Findings include mild acne, an enlarged liver and spleen, some swelling
along both tibias, and point tenderness along the right tibia.
These findings are MOST compatible with an excess ingestion of
A. vitamin A
B. vitamin B1
C. vitamin C
D. vitamin D
E. vitamin E

Question 37. Answer.

During a health supervision visit, the mother of a 4-month-old infant complains that the baby
is constipated, with hard stools being passed approximately every 5 days. The infant is
receiving 32 oz/day of cow milk formula containing 12 mg/L of iron. Results of the physical
examination are normal.
Of the following, the BEST nutritional management of this problem is to
A. change to formula containing 1.5 mg/L of iron
B. change to whole milk exclusively
C. dilute current formula by 50% with water
D. give pear juice in addition to current formula feeding
E. give rice cereal in addition to current formula feeding

Question 68. Answer.

A previously healthy 1-year-old infant who weighs 10 kg presents to your office with a fever
of 39°C (102.2°F). Her mother is very concerned about the child’s intake and asks for
guidance regarding caloric requirements during this illness.
Of the following, the BEST estimate of the child’s caloric requirements at this time is
A. 500 kcal/d plus 500 kcal due to the fever
B. 1,000 kcal/d plus 250 kcal due to the fever
C. 1,500 kcal/d
D. 1,500 kcal/d plus 250 kcal due to the fever
E. 2,000 kcal/d

Question 101. Answer.

You are evaluating a 4-year-old boy for bowing of the legs and short stature. Findings
include: creatinine, 0.4 mg/dL; calcium, 9.2 mg/dL; phos-phorus, 2.5 mg/dL; alkaline
phosphatase, 950 IU/L; intact parathyroid hormone, 40 pg/mL (normal, 10 to 60 pg/mL);
25-hydroxyvitamin D, 30 pg/mL (normal, 12 to 40 pg/mL); 1,25-dihydroxyvitamin D, 30
pg/mL (normal, 25 to 45 pg/mL); and urinary tubular reabsorption of phosphorus, 50%
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(normal, >85%).
The MOST likely cause of these findings is
A. familial hypophosphatemic rickets
B. hypophosphatasia
C. renal osteodystrophy
D. vitamin D-deficiency rickets
E. vitamin D-dependent rickets

Question 131. Answer.

The mother of a 1-week-old infant asks your advice concerning infant formula. After
receiving cow milk-based formula, her child developed hives, irritability, and vomiting. Both
the mother and older sibling received “special formulas” as infants because of milk and soy
intolerance.
Of the following, your best INITIAL recommendation is to give the infant a trial of a(n)
A. different type of lactose-containing cow milk-based formula
B. elemental formula
C. formula with hydrolyzed cow-milk proteins
D. lactose-free, cow milk-based formula
E. soy protein-based formula

Question 167. Answer.

A 5-year-old boy who has chronic renal failure is receiving recombinant human
erythropoietin. Three months ago he had a hematocrit of 32%. Current findings include:
hematocrit, 22%; hemoglobin, 7.1 g/dL; reticulocyte count, 1.5%; white blood cell count,
9,000/mm³; and intact parathyroid hormone, 60 pg/mL (normal, 10 to 60 pg/mL). Stools have
been negative for occult blood.
The MOST likely cause of this child’s anemia is
A. bone marrow fibrosis
B. gastrointestinal loss of blood
C. hemolysis
D. iron deficiency
E. production of antibodies to recombinant human erythropoietin

Question 196. Answer.

You are discussing the compositions of colostrum (produced during the first 5 days
postpartum) and mature human milk with a medical student who is examining newborns with
you in the nursery.
You are MOST likely to include the statement that, compared with mature human milk,
colostrum contains more

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A. calcium
B. calories
C. carbohydrate
D. fat
E. protein

Question 228. Answer.

A 9-year-old boy who has cystic fibrosis presents to your office with diarrhea and poor
weight gain. He has not had any pulmonary problems and receives no medications. He has
been receiving a regular diet and has been eating well. His height and weight are less than
the 5th percentile for age.
Of the following, the MOST likely cause of this patient’s growth failure is
A. biliary cirrhosis
B. colonic inflammation and stricture formation
C. insufficient caloric intake
D. malabsorption due to pancreatic insufficiency
E. small bowel infection with Giardia lamblia

Question 254. Answer.

Following surgery for malrotation, a 2-week-old infant who weighs 3.5 kg receives
parenteral nutrition that provides 120 kcal/kg per day, 5 g/kg protein per day (RDA, 2 g/kg
per day), 4 mEq/kg sodium per day, 100 mL/kg fluids per day, and other monovalent and
divalent ions. On the second post-operative day, the baby’s weight decreases to 3.2 kg. There
are no documented gastrointestinal losses.
The MOST likely cause for this weight loss is
A. inadequate caloric intake
B. increased insensible water losses
C. increased urine output due to acute renal failure
D. increased urine output due to increased solute load
E. normal weight loss in a newborn

Answers

Critique 7 Preferred Response: A

[View Question]
The gradual onset of headache, extremity pain, hepatosplenomegaly, and tibial edema in an
adolescent who has acne raises the possibility of ingestion of an excessive amount of vitamin
A. Isotretinoin, a popular oral drug for acne unresponsive to conventional therapy, is a
synthetic derivative of vitamin A. Conventional dosing regimens often lead to dryness of the
mucous membranes and xerosis; administration of larger doses can result in increased
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intracranial pressure (pseudotumor cerebri), hepatosplenomegaly, and radiographic changes
in the long bones. Bone pain at the site of these changes is common. Accordingly, it is likely
that the girl in the vignette has consumed large amounts of this vitamin A derivative. Of note,
chicken livers contain high concentrations of vitamin A and represent a significant dietary
source of vitamin A in some patients.
Toxic effects of excess vitamin B ingestion are not known. Excess vitamin C intake
can lead to nausea, diarrhea, and abdominal cramps, as experienced by individuals ingesting
megadoses of vitamin C to prevent the common cold. Nephrocalcinosis also has been
reported. Adolescents and young children who ingest large amounts of vitamin D can
experience anorexia, poor growth, and hypercalcemia. In addition to polydipsia and polyuria,
vitamin D toxicity in adults is characterized by gastrointestinal symptoms, such as nausea and
vomiting. There are no known toxic effects of excessive intake of vitamin E.
References:
Barness LA, Curran JS. Vitamins. In: Behrman RE, Kliegman RM, Nelson WE, eds. Nelson
Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co; 1996:145-151
Committee on Nutrition. Vitamins. In: Pediatric Nutrition Handbook. 4th ed. Elk Grove
Village, Ill: American Academy of Pediatrics; 1997:267-281
Hurwitz S. Acne vulgaris: pathogenesis and management. Pediatrics in Review.
1994;15:47-53
LeLeiko NS, Chao C. Vitamins. In: Rudolph AM, ed. Rudolph's Pediatrics. 20th ed.
Stamford, Conn: Appleton & Lange; 1996:1007-1010
Prose NS. Acne and related disorders. In: Rudolph AM, ed. Rudolph's Pediatrics. 20th ed.
Stamford, Conn: Appleton & Lange; 1996:924-925

Critique 37 Preferred Response: D

[View Question]
The infant described in the vignette is receiving a commercial formula that contains the
recommended concentration of iron (12 mg/L). Most parents begin to add solid foods to the
diets of infants at about 4 months of age, and the hard stools experienced by this infant most
likely result from such a dietary change. Adding rice cereal to the diet will increase the
consistency of the stool and add to the constipation. Diluting the current formula in half with
water will decrease the caloric intake of the infant precipitously, which can negatively affect
the child's growth. Long-term feeding of such diluted formula may result in hyponatremia
with associated seizures. Feeding exclusively with whole milk would not supply the
necessary nutrients for a 4-month-infant and would increase the likelihood of iron-deficiency
anemia. Constipation also can worsen when whole milk is a major component of the diet.
Formulas that contain 1.5 mg/L of iron, the so-called "low-iron formulas", have no
place in the management of infant nutrition. Infants receiving these formulas are at risk of
developing significant depletion of iron and anemia. Many people incorrectly believe that the
iron (12 mg/L) in commercial formula is responsible for constipation and, therefore, that
switching to low-iron preparations would alleviate the problem. In reality, iron rarely affects
the stool patterns. Constipation occurs when dietary changes, such as the addition of cereal,
thicken the stool. Administration of juices, particularly pear juice, along with the current
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formula can alleviate the constipation. The high content of sugar in juices acts as an osmotic
agent, pulling extracelluar fluid into the stool mass.
References:
Barness LA. Nutrition update. Pediatrics in Review. 1994;15:321-326
Committee on Nutrition. Formula feeding of term infants. In: Pediatric Nutrition Handbook.
4th ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1997:29-42

Critique 68 Preferred Response: B

[View Question]
Five major factors affect a child's energy (calorie) requirements. Basal metabolism describes
the energy expenditure used to maintain the body's metabolism at rest and while fasting.
Additional calories are needed for growth and physical activity. A small component of a
child's caloric needs are lost in the urine and stool. Finally, approximately 5% to 10% of the
calories used by a child are the result of a rise in resting metabolism that follows the
ingestion of a meal.
In the healthy child, caloric requirements can be estimated using age-specific
standards published by the Committee on Nutrition of the American Academy of Pediatrics
or by a simplified method that relates caloric requirements to body weight similar to that used
to calculate fluid requirements (Table 1). However, the most effective indicator of caloric
adequacy is the rate of weight gain or changes in body composition over time compared with
published, age-specific norms (ie, growth charts).
According to either of these methods for calculating the caloric requirements for the
child described in the vignette, the recommended daily intake would be 1,000 kcal. An
additional 250 kcal would be necessary to meet her increased caloric needs due to fever ([2°C
temperature elevation] X [12% of maintenance requirements per degree]).
Neither the recommended dietary allowances (RDA) nor the equation based on body
weight adequately identifies the caloric requirements for sick or malnourished children.
Additional calories also are needed in certain medical and surgical conditions (Table 2).
References:
Barness LA, Curran JS. Nutrition. In: Behrman RE, Kliegman RM, Nelson WE, eds. Nelson
Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co; 1996:140-143
Committee on Nutrition. Pediatric Nutrition Handbook. 4th ed. Elk Grove Village, Ill:
American Academy of Pediatrics; 1997
Forbes GB. Nutrition. In: Hoekelman RA, ed. Primary Pediatric Care. 2nd ed. St Louis, Mo:
Mosby-Year Book, Inc; 1992:168-170

Critique 101 Preferred Response: A

[View Question]
Familial hypophosphatemia is the most commonly encountered non-nutritional form of
rickets. The usual mode of inheritance is X-linked, although an autosomal dominant form has
been described. The pathogenesis of the disease is related to a renal leak of phosphate
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associated with a defect in the conversion of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin
D (calcitriol). In spite of hypophosphatemia, patients who have familial hypophosphatemia
have low to low-normal levels of calcitriol, which is a potent stimulus for this hydroxylation
process. In addition, affected patients do not respond to oral phosphate supplementation and
require calcitriol to heal the bone lesions and promote improved growth. As described in the
vignette, laboratory evaluation reveals normal serum calcium and parathyroid hormone
concentrations and elevated alkaline phosphatase levels.
Vitamin D deficiency is a nutritional disorder that is due to inadequate intake of
vitamin D, inadequate exposure to sunlight, or a combination of both factors. Patients present
with clinical or radiographic evidence of rickets associated with low phosphate levels,
low-normal to low calcium concentrations, elevated alkaline phosphatase levels, and
decreased renal tubular reabsorption of phosphate in the presence of hyperparathyroidism.
The concentration of 25-hydroxyvitamin D (which reflects the stores of vitamin D) is very
low in affected patients.
Vitamin D-independent rickets, type I occurs in patients who do not have the 1
alpha-hydroxylase enzyme in the proximal tubule and results in manifestations of nutritional
rickets. However, in these patients, the concentration of 25-hydroxyvitamin D is normal,
while 1,25-dihydroxyvitamin D levels are undetectable. Vitamin D-dependent rickets, type II
occurs in patients who have an end-organ resistance to the action of vitamin D; this results in
a markedly elevated concentration of 1,25-dihydroxyvitamin D.
Hypophosphatasia is an autosomal recessive disorder that resembles rickets
radiographically, but is associated with low levels of serum alkaline phosphatase. The disease
is heterogeneous in its severity and may be fatal.
Renal osteodystrophy is a disorder associated with chronic renal failure. The
subsequent decreased glomerular filtration rate results in a state of phosphate retention that
causes reduced activity of the 1 alpha-hydroxylase enzyme and low calcitriol levels. It is
associated with hypocalcemia, hyperphosphatemia, secondary hyperparathyroidism, and
increased serum alkaline phosphatase activity.
References:
Chesney RW. Metabolic bone disease. In: Behrman RE, Kliegman RM, Nelson WE, eds.
Nelson Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co; 1996:1984-1990
Dabbagh S. Renal osteodystrophy. Curr Opin Pediatr. 1998;10:190-196
Hanna JD, Chan JC. Renal hypophosphatemic rickets. Curr Ther Endocrinol Metab.
1997;6:533-540

Critique 131 Preferred Response: C

[View Question]
The incidence of cow milk protein allergy in the general population has been estimated to
range from 0.3% to 7%, but the incidence increases to 30% in children who have atopy.
Current theories suggest that a combination of type 1 (immediate hypersensitivity), type 3
(immune complex reaction), and type 4 (cell-mediated delayed hypersensitivity) reactions are
involved. Several milk proteins (eg, beta-lactoglobulin, lactalbumin, bovine serum albumin,
bovine serum globulin) have been found to elicit a strong allergic response. Recent data
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suggest that approximately 50% of infants who are allergic to cow milk protein also will have
intolerance to soy protein.
Symptoms of cow milk protein sensitivity typically begin within the first 6 weeks of
life, but may occur as early as 48 hours following birth or be delayed until adulthood.
Manifestations may be generalized (anaphylaxis, shock) or limited to the gastrointestinal
tract (vomiting, diarrhea, malabsorption, poor weight gain, constipation, colitis, bleeding),
the skin (lip swelling, eczema, hives, angioedema), or the respiratory tract (sneezing,
rhinorrhea, wheezing, cough, pneumonia) and may include proteinuria, edema, irritability,
headache, and joint swelling.
A complete history, thorough physical examination, and positive oral challenge are
the cornerstones for diagnosis of gastrointestinal food hypersensitivity. Laboratory tests are
helpful adjuncts in children suspected of having food protein intolerance. In infants who have
chronic diarrhea, failure to thrive, or colitis, an endoscopic evaluation to obtain a biopsy of
the affected area is indicated. Skin-prick testing is the most sensitive method for detecting
immunoglobulin E (IgE)-mediated food allergies, but skin hypersensitivity testing is not
reliable in children who are known to have abnormal delayed reactions, malabsorption, or
enteropathy. In infants who have eczema or gastrointestinal symptoms, radioallergosorbent
(RAST) testing of the blood for food-specific IgE antibodies is a useful alternative. In many
infants, cow milk protein sensitivity does not involve a type 1 (immediate hypersensitivity)
reaction, and skin testing is less reliable in these children.
Once the diagnosis of food protein is established, therapy is directed at eliminating
the food allergen(s) from the child's diet. In infants who have food hypersensitivity,
breastfeeding is advocated even more strongly than it is in healthy newborns. It is important
to emphasize that cow milk protein has been identified in human milk obtained from up to
30% of lactating mothers and may be a source of continued symptoms, even in an infant who
is breastfed exclusively. Maternal elimination of milk products or discontinuation of
breastfeeding may be necessary in such instances. The need to eliminate both milk and soy
protein from an infant's diet requires the use of a protein hydrolysate formula. Accordingly,
administration of a formula containing hydrolyzed cow milk proteins is the most appropriate
management of the child described in the vignette. Partially hydrolyzed formulas are not
appropriate for use in an allergic child because such proteins still can initiate an allergic
response. Approximately 3% of infants who exhibit a hypersensitivity to cow milk also react
to protein hydrolysate formulas; such infants require an elemental formula to control their
symptoms. Pharmacologic therapy using ketotifen, disodium cromoglycate, and inhalant
drugs is indicated in the rare instances in which dietary modification does not successfully
control the symptoms of food intolerance.
The prognosis for children who have milk and soy allergy is excellent. By 3 years of
age, 80% to 90% of such food hypersensitivities resolve. In contrast, children who are
allergic to peanuts, nuts, and fish rarely outgrow their allergies.
In an infant who has milk protein sensitivity, there is little benefit in changing from
one cow milk-based formula to another that either contains or eliminates lactose. Lactose
intolerance can cause diarrhea and vomiting in an infant, but it is not an immunologic
reaction. Similarly, use of soy formula should be avoided because there is significant
cross-reactivity between milk and soy protein in stimulating a hypersensitivity reaction.

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References:
Cantani A. Diagnostic criteria for food allergy with predominately intestinal symptoms. J
Pediatr Gastroenterol Nutr. 1993;16:476-478
James JM, Sampson HA. Immunologic changes associated with the development of tolerance
in children with cow milk allergy. J Pediatr. 1992;121:371-377
Sampson HA. Adverse reactions to foods. In: Middleton E Jr, Reed CE, Ellis EF, Adkinson
NF Jr, Yunginger JW, Busse WW, eds. Allergy: Principles and Practice. 4th ed. St Louis,
Mo: Mosby-Year Book, Inc; 1993:1661-1686
Walker WA. Summary and future directions. Adverse reactions to food in infancy and
childhood. J Pediatr. 1992;121:S4-S6

Critique 167 Preferred Response: D

[View Question]
The pathogenesis of the anemia of chronic renal failure is related primarily to inadequate
production of erythropoietin by the failing kidneys. However, nutritional deficiencies of folic
acid and iron also should be considered because most children who have chronic renal failure
have poor appetites. Treatment of the anemia includes the administration of recombinant
human erythropoietin (r-HuEPO), which stimulates erythropoiesis and increases the
hemoglobin concentration. To date, there are no reports of antibodies being formed to the
hormone. Accordingly, when a patient does not respond to r-HuEPO or has a decrease in the
hemoglobin concentration while receiving r-HuEPO, such as the boy described in the
vignette, other causes must be investigated.
The most common cause of anemia in patients who have chronic renal failure and are
receiving r-HuEPO is iron deficiency due to depletion of endogenous iron stores.
Measurement of serum ferritin and iron saturation levels is helpful to confirm this diagnosis.
Evaluation for gastrointestinal blood loss is important in patients who have anemia
and chronic renal failure. Gastrointestinal blood loss occurs at a higher frequency in patients
who have uremia because of stress, poor platelet function, and decreased concentrations of
von Willebrand factor VIII. A careful history should be obtained, and stool guaiac tests for
occult blood should be performed. However, in a patient who has had multiple stools
negative for occult blood, gastrointestinal blood loss would be less likely than iron deficiency
anemia.
The low reticulocyte count described in the vignette makes hemolysis unlikely. Bone
marrow fibrosis occurs in patients who have severe secondary hyperparathyroidism, and the
serum parathyroid hormone level is normal in this patient.
Administration of oral iron supplementation should restore the effectiveness of
r-HuEPO. It should not be administered with alkali, phosphate binders, or dairy products, all
of which decrease its absorption. Patients should be encouraged to ingest the iron on an
empty stomach. If there are no problems with potassium metabolism, iron can be
administered with 1 oz of orange juice, which increases gastrointestinal absorption.
References:
Bergstein JM. Chronic renal failure. In: Behrman RE, Kliegman RM, Nelson WE, eds.
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Nelson Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co; 1996:1518-1521
Warady BA, Jabs K. New hormones in the therapeutic arsenal of chronic renal failure.
Growth hormone and erythropoietin. Pediatr Clin North Am. 1995;42:1551-1577

Critique 196 Preferred Response: E

[View Question]
Colostrum, the milk produced by women in the first 5 days postpartum, is richer in protein
than milk collected during the later stages of lactation. The protein concentration of
colostrum is approximately 2.3 g/dL and that of mature milk is 1.2 g/dL. The whey proteins
comprise the largest fraction (about 70%) of human milk proteins, and the caseins account
for the remainder. The major whey protein in human milk is alpha-lactalbumin. This is the
principle nutritional protein of human milk because it facilitates gastric emptying, is easy to
digest, and is absorbed rapidly. Lactoferrin, lysozyme, and secretory immunoglobulin A are
the other whey proteins in human milk, and they play important roles in host defense. The
caseins, which give human milk its characteristic white appearance, coagulate readily into
curds in the stomach, which lessens their nutritional value relative to the whey proteins.
Fat is the most variable macronutrient in human milk. It changes with the stage of
lactation, on a diurnal basis, and within a single feeding. The fat concentration of colostrum
is low (approximately 1.7 g/dL) compared with the more than twofold higher concentration
of mature milk (approximately 4.0 g/dL). The fat in human milk consists primarily of very
long-chain fatty acids, which include arachidonic acid and docosahexaenoic acid. These fatty
acids are derived from linoleic and linolenic acids and appear to be important in cognition,
growth, and vision.
Lactose is the principle carbohydrate in human milk, and it is the least variable of all
nutrients. The lactose concentration of colostrum is approximately 6.0 g/dL compared with
7.0 g/dL for mature milk. Small quantities of unabsorbed lactose from human milk feedings
result in a soft stool consistency, proliferation of nonpathogenic bacteria in the fecal flora,
and improved absorption of minerals.
Using caloric equivalents of 4.0 kcal/g protein, 9.0 kcal/g fat, and 4.0 kcal/g of
carbohydrate, the energy content of colostrum is estimated at 49 kcal/dL and that of mature
milk is 69 kcal/dL.
In contrast to the changing concentrations of protein, fat, and carbohydrate in human
milk during lactation, concentrations of minerals, calcium, and phosphorus are relatively
constant throughout lactation. The approximate concentration of calcium is 30 mg/dL and
that of phosphorus is 14 mg/dL in human milk.
References:
American Academy of Pediatrics. Committee on Nutrition. Nutrition and lactation.
Pediatrics. 1981;68:435-443
Schanler RJ, Butte NF. Rationale for breast-feeding. In: Tsang RC, Zlotkin SH, Nichols BL,
Hansen JW, eds. Nutrition During Infancy: Principles and Practice. 2nd ed. Cincinnati,
Ohio: Digital Educational Publishing, Inc; 1997:357-380

Critique 228 Preferred Response: D

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[View Question]
Children who have cystic fibrosis (CF) are at increased risk for malnutrition, which can have
adverse effects on growth and development, body image, emotional well-being, immune
status, and pulmonary function. Three factors contribute to the pathogenesis of malnutrition
in these children: malabsorption, increased energy requirements, and decreased caloric
intake.
Pancreatic insufficiency due to obstruction of intrapancreatic ductules by tenacious
secretions is the hallmark of CF. The pancreatic destruction begins in utero, but the extent of
the damage varies, which accounts for the differences in clinical presentation. It is present at
birth in 50% of children who have CF; an additional 35% to 40% are affected by 9 years of
age. The severity of pancreatic insufficiency is associated with the specific genotype of the
affected individual. For example, absence of the CF transmembrane regulator gene located at
position F508 on chromosome 7 almost always is associated with severe pancreatic
dysfunction. Children who have other genotypes may have normal pancreatic function.
Pancreatic insufficiency results in inadequate production of lipase, amylase, and proteases,
with subsequent malabsorption of fats, carbohydrates, and proteins. Accordingly,
malabsorption due to pancreatic insufficiency is the most likely cause of growth failure in the
9-year-old child described in the vignette.
A small increase in energy expenditure has been documented in children who have
CF that is due to the genetic and metabolic defect itself. Children who experience chronic
sinopulmonary infections, respiratory insufficiency, and malnutrition are reported to have
energy expenditures ranging from 85% to 153% of predicted compared with age-, gender-,
and weight-matched controls. Increased energy expenditure also has been associated with
long-term requirements for bronchodilator therapy.
The average caloric intake of children who have CF is equal to the intake of
age-matched controls. However, during periods of anorexia and vomiting due to pulmonary
exacerbations and abdominal pain due to pancreatitis, esophagitis, or hepatobiliary disease,
caloric intake will be decreased. Inappropriate use of unpalatable low-fat diets to prevent
malabsorption also may limit the child's caloric intake. The boy described in the vignette is
reported to be eating well, so insufficient caloric intake is less likely to be the cause of the
growth failure.
Because of the potential for decreased caloric intake during exacerbations of CF,
nutritional management should be directed at providing 120% to 150% of the recommended
dietary allowance for gender and age. Foods high in fat content should be encouraged, and
the diet should be as normal for age as possible. In patients who have CF, the cornerstone of
nutritional therapy is pancreatic enzyme replacement, which minimizes malabsorption and
allows normal growth and weight gain. Pancreatic enzymes should be taken at regular
intervals throughout the day with meals and snacks. The doses of the enzyme replacement
should be individualized to control steatorrhea. In some children, histamine-2 receptor
antagonist therapy is needed to optimize the pancreatic replacement therapy. Children who
cannot maintain adequate weight gain using supplemental oral feedings and optimized
enzyme replacement are candidates for enteral feedings via a nasogastric, gastrostomy, or
jejunostomy tube or parenteral hyperalimenation.
Biliary cirrhosis contributes to malabsorption by decreasing the bile flow required for
fat absorption. No specific therapy is available for this condition, although successful
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reduction of steatorrhea with pancreatic enzyme replacement has been shown to increase the
total bile acid pool and decrease fecal bile acid excretion. Colonic inflammation and stricture
formation may result from excessive pancreatic enzyme replacement and should have only a
limited effect on a child's overall nutritional balance. Children who have CF are no more
likely than other children to become infected with Giardia lamblia.
References:
Levy LD, Durie PR, Pencharz PB, Corey ML. Effects of long-term nutritional rehabilitation
on body composition and clinical status in malnourished children and adolescents with cystic
fibrosis. J Pediatr. 1985;107:225-230
Ramsey BW, Farrell PM, Pencharz P. Nutritional assessment and management in cystic
fibrosis: a consensus report. The Consensus Committee. Am J Clin Nutr. 1992;55:108-116
Rettammel AL, Marcus MS, Farrell PM, Sondel SA, Koscik RE, Mischler EH. Oral
supplementation with a high-fat, high energy product improves nutritional status and alters
serum lipids in patients with cystic fibrosis. J Am Diet Assoc. 1995;95:454-459
Vaisman N, Pencharz PB, Corey M, Canny GJ, Hahn E. Energy expenditure of patients with
cystic fibrosis. J Pediatr. 1987;111:496-500

Critique 254 Preferred Response: D

[View Question]
The rate of water excretion by the kidney depends on the solute load that must be excreted,
the kidney's concentrating ability, and the water intake. The renal solute load is derived from
protein and electrolytes provided in the diet or the metabolism and catabolism of endogenous
tissue. Although the adult kidney is capable of concentrating the urine up to an osmolality of
1,200 mOsm/kg H20, the infant's kidney cannot achieve this. The maximum concentrating level achieved in a term
infant ranges from 380 to 800 mOsm/kg H20 following water deprivation.

As described in the vignette, when an infant has to handle a high solute load due to
increased protein intake compounded by a high rate of catabolism, which may occur in
periods of stress (eg, surgery, sepsis), polyuria may develop. If the fluid intake is limited,
dehydration may ensue. The infant described in the vignette is receiving an adequate caloric
intake for age and has no evidence of renal failure or clinical evidence of increased insensible
water losses. Normal weight loss of the newborn period generally occurs in the first few days
after birth; by 10 days of age, most infants have regained their birthweights.
References:
Levine SD. Concentrating and diluting mechanisms. In: Edelmann CM Jr, ed. Pediatric
Kidney Disease. 2nd ed. Boston, Mass: Little, Brown and Co; 1992:185-200
Sulyok E. Postnatal adaptation. In: Holliday MA, Barratt TM, Avner ED, eds. Pediatric
Nephrology. 3rd ed. Baltimore, Md: Williams & Wilkins; 1994:267-286

1998 Self-Assessment Exercise —

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[Return to Category List]

Questions [Print Directions](4)

Question 1. Answer.
A 4-week-old boy who was born at 28 weeks' gestation and weighed 800 g at birth is gaining
weight at a rate of only 5 g/day even though his caloric intake is 125 kcal/kg. The stool is
poorly formed and bulky. The infant is receiving a lactose-free formula containing
24 kcal/oz.
Which of the following interventions is MOST likely to result in a decrease in steatorrhea and
improved weight gain?
A. Increase the daily caloric intake to 150 kcal/kg
B. Increase the glucose polymers in the formula
C. Increase the protein intake
D. Increase vitamin A and vitamin E supplements
E. Substitute medium-chain triglycerides for long-chain triglycerides

Question 21. Answer.

Which of the following drugs administered to the mother is MOST likely to have an adverse
effect on the infant who is breastfeeding?
A. Acetaminophen
B. Diazepam
C. Furosemide
D. Gentamicin
E. Penicillin

Question 38. Answer.

A 14-year-old female adolescent who has severe juvenile rheumatoid arthritis presents to
your office with epigastric abdominal pain. Six weeks earlier she began taking a nonsteroidal
anti-inflammatory drug (NSAID) because of worsening joint complaints.
Of the following, the most appropriate INITIAL management of her symptoms would be
A. administration of an antibiotic effective against Helicobacter pylori
B. administration of an H2-receptor antagonist
C. dietary modification
D. substitution of salicylate for NSAID
E. upper endoscopy and gastric biopsy for gastric adenocarcinoma

Question 56. Answer.

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The essential difference between elemental formulas and casein hydrolysate formulas is that
elemental formulas are MOST likely to include
A. a hyperosmolar composition
B. an increased concentration of vitamins and minerals
C. lactose as the predominant carbohydrate source
D. medium-chain triglycerides
E. protein in the form of amino acids rather than oligopeptides

Question 58. Answer.

Among the following, the MOST common cause of urticaria is
A. cold exposure
B. complement factor H deficiency
C. exercise
D. ingestion of foods and food additives
E. sun exposure

Question 78. Answer.

A 5-week-old girl who has Down syndrome and a complete atrioventricular septal defect
weighed 3.5 kg at birth; she now weighs 3.8 kg. She is receiving digoxin, furosemide, and
captopril. She is restricted to 400 mL/day of 30 cal/oz fortified human milk. Findings
include: pulse, 155 beats/min; respirations, 45 breaths/min; blood pressure, 80/55 mm Hg;
intercostal retractions; and hepatomegaly.
This infant's poor weight gain MOST likely is due to
A. dehydration from diuretic therapy
B. inadequate caloric intake
C. parental neglect
D. toxicity associated with captopril
E. toxicity associated with digoxin

Question 98. Answer.

Among the following disorders, rickets is MOST likely to develop in patients who have
A. acute pancreatitis
B. adrenal insufficiency
C. cirrhosis
D. congenital heart disease
E. lactose intolerance

Question 117. Answer.

A 6-month-old boy developed a weepy, crusted dermatitis around the eyes, nose, mouth,
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diaper area, hands, and feet about 4 weeks after being weaned from human milk to formula.
He is listless, recently developed diarrhea, and has stopped gaining weight. In addition to the
dermatitis, he has sparse hair that is fine and lightly pigmented.
Of the following, this constellation of findings is MOST consistent with a deficiency in
A. copper
B. thiamine
C. vitamin A
D. vitamin C
E. zinc

Question 138. Answer.

Following an acute febrile illness, a 6-month-old infant has had diarrhea for 3 weeks. When
the diarrhea began, the mother said she fed the infant an oral electrolyte solution exclusively.
As the diarrhea slowed, the mother reintroduced cow milk infant formula, and the diarrhea
recurred. The infant continues to receive oral electrolyte solution exclusively. She appears
thin but is otherwise healthy.
The BEST management at this time is to administer
A. a gluten-free diet
B. a hypoallergenic diet
C. a lactose-free diet
D. clindamycin
E. metronidazole

Question 157. Answer.

A 5-month-old infant who was bottle fed cow milk-based formula had severe watery diarrhea
for 4 days. It resolved within 24 hours of beginning an oral rehydration solution. Efforts to
restart the previous formula result in a return of severe diarrhea.
At this time, you are MOST likely to recommend a 5-day course of
A. elemental formula
B. evaporated milk
C. goat milk
D. lactose-free formula
E. oral rehydration solution

Question 176. Answer.

In which of the following conditions is intermittent (bolus) feeding PREFERRED to
continuous nasogastric feeding?
A. Congenital heart disease with failure to thrive
B. Gastroesophageal reflux with failure to thrive
C. Inflammatory bowel disease with bloody diarrhea
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D. Malabsorption syndrome with severe villous atrophy
E. Oromotor discoordination due to birth asphyxia

Question 196. Answer.

In the preterm infant, supplementation of human milk or use of formulas containing
increased concentrations of fat and protein often is necessary for adequate nutrition.
Of the following, the BEST explanation for this need for supplementation is that
A. amino acids are poorly absorbed in the preterm infant
B. bile acid production in the preterm infant is normal but pancrease activity is deficient
C. fat in human milk is of low caloric value
D. malabsorption of up to 20% of ingested fat is common in the preterm infant
E. medium-chain triglycerides are poorly absorbed in the preterm infant

Question 216. Answer.

Impaired breastfeeding in the first few weeks of life can be related to both neonatal and
maternal conditions.
Of the following, the MOST likely maternal reason for unsuccessful breastfeeding is
A. candidiasis
B. contact dermatitis
C. fibrocystic breast disease
D. inverted nipples
E. mastitis

Question 236. Answer.

The average capillary hematocrit value that would be considered normal for a term infant
during the first three days of life is CLOSEST to
A. 38%
B. 44%
C. 50%
D. 56%
E. 62%

Question 253. Answer.

A 6-month-old infant who has congenital heart disease has grown poorly due to insufficient
caloric intake. You recommend nasogastric feeding to enhance weight gain.
Of the following, the MOST common complication of nasogastric feeding is
A. allergic reaction to the nasogastric tube
B. dehydration due to diarrhea
C. gastric perforation
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D. gastritis
E. gastroesophageal reflux

Answers

Critique 1 Preferred Response: E

[View Question]
The bile acid pool of the human neonate is very small compared with the adult, and fecal
losses of bile acids are excessive in the neonate. Especially in the preterm infant, the level of
intraluminal bile acids may fall below the critical micellular concentration, resulting in a
physiologic steatorrhea. Substituting medium-chain triglycerides (MCT) for long-chain
triglycerides will decrease the steatorrhea and enhance weight gain because MCT do not
require bile acids for absorption.
Increasing the daily caloric intake to 150 kcal/kg of formula without decreasing the
amount of long-chain triglycerides will accentuate the problem of steatorrhea. Increasing the
carbohydrate concentration of the formula with glucose polymers or increasing the protein
intake also will increase the daily caloric intake, but will not decrease the steatorrhea. Fecal
losses of vitamins A, D, E, and K, which are fat-soluble, increase with steatorrhea, but
additional supplementation of these vitamins will not decrease the steatorrhea or enhance
weight gain.
Recognizing that the preterm infant can develop a physiologic steatorrhea,
manufacturers of formula designed for these neonates have substituted MCT for long-chain
triglycerides. Additionally, vitamin concentrations in these formulas have been adjusted to
provide the optimal amount based on the volume expected to be ingested by the preterm
infant. MCT also may be added to the formula simply to increase the caloric content.
References:
Barness LA, Curran JS. Formula feeding. In: Nelson WE, Behrman RE, Kliegman RM,
Arvin AM, eds. Nelson Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co;
1996:156-163
Belknap WM, McEvoy C. Developmental disorders of gastrointestinal function. In: Oski FA,
DeAngelis CD, Feigin RD, McMillan JA, Warshaw JB, eds. Principles and Practice of
Pediatrics. 2nd ed. Philadelphia, Pa: JB Lippincott Co; 1994:415-423
Bucuvalas JC, Balistreri WF. Bile acid metabolism. In: Rudolph AM, Hoffman JIE, Rudolph
CD, eds. Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange;
1996:1126-1127
Byrne WJ. Fat digestion and absorption. In: Taeusch HW, Ballard RA, Avery ME, eds.
Schaffer & Avery's Diseases of the Newborn. 6th ed. Philadelphia, Pa: WB Saunders Co;
1991:660-661
Vanderhoof JA, Zach TL, Adrian TE. Gastrointestinal disease. In: Avery GB, Fletcher MA,
MacDonald MG, eds. Neonatology: Pathophysiology and Management of the Newborn.
Philadelphia, Pa: JB Lippincott Co; 1994:605-629

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Critique 21 Preferred Response: B
[View Question]
In most instances, drugs administered to a nursing mother are not excreted in sufficient
amounts in milk to affect the breastfeeding infant. Further, even if the drug is excreted in
high concentrations in human milk, it often is not absorbed well by the infant. Diazepam,
however, is both sufficiently concentrated in human milk and absorbed by infants to produce
the systemic effect of sedation in the neonate. This is not true for acetaminophen, furosemide,
gentamicin, or penicillin.
Radionuclides generally should not be administered to mothers who are
breastfeeding. On the other hand, if the half-life of an isotope is short, such as for
technetium-99, which has a half-life of 6 hours, the mother can stop breastfeeding for 24 to
36 hours after receiving the isotope, then resume feeding when any danger of the infant
absorbing it has passed. Antimetabolites, such as methotrexate, also are contraindicated.
If the mother who is breastfeeding requires a particular drug, the prescribing
physician first should determine if there are alternative therapies to that medication. If not,
the effect on the neonate can be diminished by administering the medication to the mother
immediately after she has nursed the infant.
References:
American Academy of Pediatrics Committee on Drugs. The transfer of drugs and other
chemicals into human milk. Pediatrics. 1994;93:137-150
Freed GL, Clark SJ. Breastfeeding and maternal illness. Contemporary Pediatrics.
1996;13:49-61
Gutierrez-Pickett AC, Hurley A. Appendix 1, Drugs. In: Taeusch HW, Ballard RA, Avery
ME, eds. Schaffer & Avery's Diseases of the Newborn. 6th ed. Philadelphia, Pa: WB
Saunders Co; 1991:1055-1056
Kliegman RM. Parent-infant bonding. In: Nelson WE, Behrman RE, Kliegman RM, Arvin
AM, eds. Nelson Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co;
1996:439-440
Zenk KE. Drug use and breast-feeding. In: Rudolph AM, Hoffman JIE, Rudolph CD, eds.
Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange; 1996:802-803

Critique 38 Preferred Response: B

[View Question]
Acute and chronic ingestion of nonsteroidal anti-inflammatory drugs (NSAIDs) has been
associated with gastritis and mucosal ulceration that can result in upper gastrointestinal blood
loss. Gastric erosions are found in 30% to 50% of adult patients receiving chronic NSAID
therapy, and ulcers (both gastric and duodenal) occur in approximately 25%. Serious
complications of NSAID use are identified in 2% to 4% of long-term users.
The toxic consequences of NSAID use are the result of both direct topical injury and
systemic effects. As potent inhibitors of prostaglandin synthesis, NSAIDs decrease mucosal
bicarbonate and mucus production, reduce mucosal blood flow, interfere with neutrophil
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adherence, and inhibit gastric acid production. Enterohepatic recirculation of NSAIDs also
may be important in the development of mucosal injury. The effects of NSAIDs upon platelet
aggregation further potentiate bleeding and may interfere with the normal healing process of
the upper gastrointestinal tract.
There appears to be no relationship between the development of NSAID-induced
ulceration and infection with Helicobacter pylori, so administration of an antibiotic against
this pathogen would not be helpful. Aspirin is as toxic as NSAIDs in promoting
gastroduodenal inflammation, so substitution of salicylate would not be appropriate.
Dyspeptic symptoms are quite common in patients receiving NSAID therapy.
However, there are no clinical indicators to differentiate patients who only have dyspepsia
from those who have ulcerations. Indeed, patients who have NSAID-associated ulcers are
less likely to be symptomatic than patients who have ulcers and have not received NSAID
therapy.
Given the efficacy of pharmacologic therapy for peptic ulcer disease, there is little
reason to rely on dietary modification as the primary intervention in such patients. In patients
who have NSAID-induced ulcers. H2-receptor antagonists (eg, famotidine, ranitidine) are
appropriate therapy. If the NSAID can be discontinued at the same time, response to
conventional doses of H2-receptor antagonists usually is rapid. However, if NSAID therapy
must be maintained, only 50% to 60% of patients will be healed following 8 weeks of
H2-receptor antagonist therapy.
Omeprazole, a proton pump inhibitor that affords greater suppression of gastric acid,
may be more effective in healing gastric ulcers in patients who must continue NSAIDs. The
efficacy and safety of omeprazole in the pediatric population has not been established, but
initial studies suggest an efficacy and safety profile similar to adults. Misoprostol and
sucralfate are mucosal protective agents that are effective in the treatment of gastric ulcers,
but neither appears to be particularly effective in healing ulcers when the NSAID is
continued. Prophylactic administration of H2-receptor antagonists and misoprostol have been
effective in preventing duodenal ulcers associated with NSAID use, but only misoprostol has
been found to reduce the incidence of gastric ulcers.
The extremely low incidence of gastric malignancy in the pediatric population
obviates the need for endoscopy in the initial management of a child suspected of having a
gastric ulcer. Endoscopic evaluation of the stomach is reserved for those who fail to respond
to an initial course of H2-receptor antagonist or omeprazole therapy. If endoscopy is
performed, assessment for the presence of H pylori should be undertaken (eg, staining of the
biopsy for urease active, mucosal culture). Generally, noninvasive testing (eg, serologic
testing for antibodies to H pylori and urea breath testing) are the initial diagnostic studies
performed in a patient who has suspected gastroduodenitis caused by H pylori.
References:
Ehsanullah RS, Page MC, Tildesley G, Wood JR. Prevention of gastroduodenal damage
induced by non-steroidal anti-inflammatory drugs: controlled trial of ranitidine. BMJ.
1988;297:1017-1021
Fromm D. How do non-steroidal anti-inflammatory drugs affect gastric mucosal defenses?
Clin Invest Med. 1987;10:251-258
Graham DY, Agrawal NM, Roth SH. Prevention of NSAID-induced gastric ulcer with
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misoprostol: multicentre, double-blind, placebo-controlled trial. Lancet. 1988;2:1277-1280
Lanza F, Peace K, Gustitus L, Rack MF, Dickson B. A blind endoscopic comparative study
of misoprostol versus sucralfate and placebo in the prevention of aspirin-induced gastric and
duodenal ulceration. Am J Gastroenterol. 1988;83:143-146
McCarthy DM. Nonsteroidal antiinflammatory drug-induced ulcers: management by
traditional therapies. Gastroenterology. 1989;96:662-674
Soll AH, Weinstein WM, Kurata J, McCarthy D. Nonsteroidal anti-inflammatory drugs and
peptic ulcer disease. Ann Intern Med. 1991;114:307-319
Walan A, Bader JP, Classen M, et al. Effect of omeprazole and ranitidine on ulcer healing
and relapse rates in patients with benign gastric ulcer. N Engl J Med. 1989;320:69-75

Critique 56 Preferred Response: E

[View Question]
Currently, five specialized formulae are available for infants: Nutramigen® (Mead Johnson),
Alimentum® (Ross Laboratories), Pregestamil® (Mead Johnson), Neocate® (SHS), and
Good Start® (Carnation). All of these infant formulas have comparable concentrations of
minerals and vitamins.
The protein hydrolysate formulas (eg, Nutramigen®, Alimentum®) are indicated for
infants who have an allergy to either intact milk protein or soy protein isolates. Elemental
formulas (eg, Pregestamil®, Neocate®) are used routinely in children who are allergic to the
protein hydrolysate formulas or who have a generalized malabsorption syndrome (ie, cystic
fibrosis or short bowel syndrome). The essential difference between elemental formulas and
casein hydrolysate formulas is that elemental formulas are most likely to include protein in
the form of amino acids rather than oligopeptides.
Nutramigen® contains casein hydrolyzed to amino acids and small polypeptides. The
osmolarity of 20 kcal/oz of Nutramigen® is 480 mOsm/L, and it is lactose-free, containing
sucrose (72%) and tapioca starch (28%).
The protein and carbohydrate sources of Alimentum® are similar to Nutramigen®,
with 60% of the protein available as free amino acids with added carnitine and taurine.
Alimentum® contains medium-chain triglycerides (MCT) (50% of fat content) as well as
safflower (40%) and soy (10%) oils. The osmolarity of 20 kcal/oz of Alimentum® is 370
mOsm/L.
Pregestamil® is considered an elemental formula for infants. It contains casein
hydrolyzed to free amino acids with added cystine, tyrosine, and tryptophan. Its sources of fat
are corn oil (60%) and MCT (40%). Carbohydrate is provided by corn syrup solids (85%)
and modified tapioca starch (15%). The osmolarity of 20 kcal/oz of Pregestamil® is 350
mOsm/L.
Neocate® is the newest of the elemental formulas. It contains casein hydrolyzed
completely to free amino acids. Corn syrup solids serve as the carbohydrate source, and the
fat sources are safflower oil and vegetable oil (coconut and soy). The osmolarity of 20
kcal/oz of Neocate® is 342 mOsm/L.
Good Start® contains hydrolyzed whey protein in the form of small polypeptides and
includes 100 to 700 times the number of identifiable milk protein antigens as Nutramigen®
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and Alimentum®. The osmolarity of 20 kcal/oz of Good Start® is 260 mOsm/L. The
carbohydrate sources are lactose (70%) and maltodextrins (30%).
References:
Barness LA. Nutrition update. Pediatrics in Review. 1994;15:321-326
Committee on Nutrition. Formula feeding of term infants. In: Pediatric Nutrition Handbook.
3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1993:11-22
Greer FR. Formulas for the healthy term infant. Pediatrics in Review. 1995;16:107-113
Klish WJ. Special infant formulas. Pediatrics in Review. 1990;12:55-62

Critique 58 Preferred Response: D

[View Question]
Urticaria, or hives, is a common skin disorder characterized by well-circumscribed but
occasionally coalescent, localized, or generalized erythematous raised skin lesions (welts) of
various sizes. The lesions usually are pruritic. Angioedema involves the deeper layers of skin
or submucosa. The distinction between urticaria and angioedema frequently is not clear; the
lesions appear to differ only in the depth of tissue involvement.
As many as 20% of people experience urticaria at some time, although it is somewhat
more common in females than males. The etiology of both urticaria and angioedema
frequently is obscure, but the most common cause of hives is ingestion of specific foods, food
additives, or drugs. The most frequently implicated foods are fish, shellfish, nuts, eggs, and
peanuts. Food additives that have been linked with hives include tartrazine, azo dyes, and
benzoates. Hives also are associated commonly with infections.
Exposure to cold can lead to "cold" urticaria. Solar urticaria is uncommon and may be
caused by various wavelengths of light. Hives and bronchospasm may be induced by
exercise, and sometimes exercise combined with the recent ingestion of certain foods can
cause symptoms of anaphylaxis.
A rare cause of urticaria is found in patients who have genetic deficiencies of factor H
or factor I of the complement system. Patients who have these defects excrete large amounts
of histamine. The defects are inherited as autosomal recessive traits.
References:
Greaves MW. Chronic urticaria. N Engl J Med. 1995;332:1767-1772
Rosen FS. Urticaria, angioedema, and anaphylaxis. Pediatrics in Review. 1992;13:387-390
Sly RM. Urticaria-angioedema. In: Nelson WE, Behrman RE, Kliegman RM, Arvin AM, eds.
Nelson Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co; 1996:644-646

Critique 78 Preferred Response: B

[View Question]
Infants who have congestive heart failure have increased work of breathing, delayed gastric
emptying, and increased caloric needs. Weight gain frequently is not adequate in these
infants when they receive a normal daily caloric intake of 110 to 120 kcal/kg body weight.
The infant in the vignette is receiving 105 kcal/kg per day. Improved weight gain has been
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demonstrated when such patients are given 150 to 160 kcal/kg. Accordingly, the poor weight
gain for the infant in the vignette probably is due to inadequate caloric intake. Use of
continuous nasogastric feeding can decrease energy expenditure and enhance weight gain.
Although dehydration as a result of diuretic therapy can account for short-term poor
weight gain, it usually is associated with low blood pressure, poor perfusion, lethargy, and
sinus tachycardia.
Parental neglect always is a possibility in infants who are failing to thrive. In fact,
neglect or abuse of children occurs more frequently in children who have any handicapping
condition, such as Down syndrome. However, in this infant, inadequate caloric intake is a
more likely explanation for poor weight gain.
Toxicities or adverse effects of captopril include hypotension, cough, rash, worsening
renal failure, hyperkalemia, and rarely leukopenia, but not poor weight gain.
Toxicities or adverse effects of digoxin include nausea, vomiting, anorexia, and
arrhythmias. Although these gastrointestinal problems can contribute to poor weight gain,
none of these symptoms is reported for the infant in the vignette.
References:
Gingell RL, Hornung MG. Growth problems associated with congenital heart disease in
infancy. In: Lebenthal E, eds. Textbook of Gastroenterology and Nutrition in Infancy. 2nd ed.
New York, NY: Raven Press; 1989:639-649
Schwarz SM, Gewitz MH, See CC, et al. Enteral nutrition in infants with congenital heart
disease and growth failure. Pediatrics. 1990;86:368-373

Critique 98 Preferred Response: C

[View Question]
Rickets is characterized by a failure of bone or osteoid mineralization because of an
unavailability or deficiency of either calcium or phosphorus, the two minerals needed for
hydroxyapatite formation. Vitamin D plays an essential role in calcium homeostasis by
stimulating calcium absorption by the small intestine. Vitamin D can be synthesized in the
skin through an ultraviolet light-dependent pathway or may be ingested as a fat-soluble
vitamin. Once in circulation, vitamin D is hydroxylated in the 25 position by hepatic cells
and subsequently in the 1 position in the kidney to form 1,25-hydroxy vitamin D. The latter is
the active agent that allows the intestine to absorb calcium.
Abnormalities in vitamin D levels can result from several conditions. In patients who
have severe liver disease, such as cirrhosis, 25-hydroxylation of vitamin D may be impaired.
Fat malabsorption also may occur in this population, but it does not appear to play a
significant role in the development of rickets. Bone mineralization is reduced as a
complication of cholestatic liver disease; this parallels the progression of the liver disease and
the patient's increasing age. Of note, the concentrations of vitamin D and its metabolites may
not correlate with the severity of the osteopenia. High doses of vitamin D or 25-hydroxy
vitamin D are successful in treating rickets in patients who have severe liver disease.
Nutritional deprivation associated with low serum vitamin D concentrations can be
caused by prematurity, malabsorption syndromes, and the administration of anticonvulsant
drugs. Patients who have pancreatic insufficiency due to cystic fibrosis are at risk for rickets
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because of fat malabsorption, but vitamin D homeostasis rarely is associated with acute
pancreatitis. Genetic disorders, including deficiency of 25 hydroxy-1 hydroxylase in the
kidney and mutations in the 1,25 dihydroxy vitamin D receptor, as well as chronic renal
disease result in vitamin D-dependent rickets.
The adrenal gland, although active in many of the pathways of steroid metabolism,
does not play a role in vitamin D metabolism, and its impairment is not associated with
rickets. Neither congenital heart disease nor lactose intolerance are associated with rickets.
References:
Argao EA, Specker BL, Heubi JE. Bone mineral content in infants and children with chronic
cholestatic liver disease. Pediatrics. 1993;91:1151-1154
Heubi JE, Tsang RC, Steichen JJ, Chan GM, Chen I-W, DeLuca HF. The use of 1,25
dihydroxycholecalciferol [1,25-(OH)2D3] in the treatment of rickets with neonatal liver
disease. J Pediatr. 1978;93:312
Kooth SW, Jones G, Reilly BJ, Fraser D. Pathogenesis of rickets in chronic hepatobiliary
disease in children. J Pediatr. 1979;94:870-874
Reichel H, Koeffler HP, Norman AW. The role of the vitamin D endocrine system in health
and disease. N Engl J Med. 1989;320:980-991
Sokol RJ. Fat-soluble vitamins and their importance in patients with cholestatic liver
diseases. Gastroenterol Clin North Am. 1994;23:673-705
Specker BL, Tsang RC. Vitamin D in infancy and childhood: factors determining vitamin D
status. Adv Pediatr. 1986;33:1-22

Critique 117 Preferred Response: E

[View Question]
The 6-month-old infant in the vignette exhibits the characteristic symptoms of zinc
deficiency, which include diarrhea, hair loss, skin rash, poor growth, listlessness, and light
pigmentation. Because human milk, which contains a protein that facilitates zinc absorption
that is not present in formula or cow milk, the onset of symptoms after the infant is weaned
from human milk makes a diagnosis of acrodermatitis enteropathica (AE) most likely. This
autosomal recessive disorder of zinc metabolism is caused by a defective transport protein in
the gastrointestinal tract that is responsible for absorption of dietary zinc. Defective activity
of zinc-dependent enzymes also results in immune dysfunction (eg, anergy,
hypogammaglobulinemia, abnormal cellular immunity, leukocyte dysfunction). Chronic
dermatitis and erosions, particularly around body orifices and creases, frequently become
secondarily infected with Candida and bacteria.
The diagnosis of AE can be made by finding abnormally low serum zinc levels.
However, care must be taken when sending blood samples for evaluation of zinc levels
because rubber-stoppered tubes and anticoagulant may be contaminated with zinc. Once the
diagnosis is confirmed, a therapeutic trial of oral zinc supplementation usually results in
rapid clearing of the skin rash and other symptoms.
Patients who have other disorders that result in chronic gastrointestinal malabsorption
(eg, cystic fibrosis, celiac disease) also can develop zinc deficiency and its associated
symptoms. Patients who have deficiencies of essential fatty acids and biotin may have a
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similar clinical presentation.
Although an isolated vitamin deficiency is rare, specific disorders have been
identified. Copper deficiency can cause refractory anemia and osteoporosis, but it has not
been associated with specific cutaneous findings. Thiamine deficiency leads to beriberi.
Nonspecific findings of beriberi include fatigue, apathy, irritability, depression, and
abdominal pain. Progressive cardiac failure and neurologic dysfunction can result in coma
and death. Children appear pale, edematous, and listless, and the skin may be waxy.
The skin becomes dry and cracked in vitamin A deficiency. Follicular hyperkeratosis
(phrynoderma) can develop on the shoulders, buttocks, and distal extremities. White mucosal
patches appear in the mouth. Vitamin A deficiency also is associated with night blindness,
corneal and conjunctival dryness, and mental and physical retardation. Vitamin C deficiency
leads to scurvy. Oral changes of scurvy include bluish-purple spongy gums, hemorrhage, loss
of periodontal bone, and eventual loss of teeth. Follicular hyperkeratosis, with broken
corkscrew hairs and perifollicular hemorrhage, are early cutaneous findings.
References:
Oleske JM, Westphal ML, Shore S, Gorden D, Bogden JD, Nahmias A. Zinc therapy of
depressed cellular immunity in acrodermatitis enteropathica. Its correction. Am J Dis Child.
1979;133:915-918
Slonim AE, Sadick N, Pugliese M, Meyers-Seifer CH. Clinical response of alopecia,
trichorrhexis nodosa, and dry, scaly skin to zinc supplementation. J Pediatr.
1992;121:890-895

Critique 138 Preferred Response: C

[View Question]
The situation described in the vignette occurs commonly in children who have acute
gastroenteritis. The initial appearance of the diarrheal stools prompted the mother to
administer an electrolyte solution, and slowing of the diarrhea reinforced that action. When
cow milk was reintroduced and the diarrhea resumed, the mother assumed that offering
electrolyte solution again would resolve the problem. Unfortunately, the etiology of the
second bout of diarrhea involved mucosal injury from the initial episode of infectious
enteritis.
Lactase exists within the brush border of the small bowel, and its activity is decreased
dramatically when the mucosal border is injured by infection (eg, acute gastroenteritis) or
ischemia. As a result, lactose (a disaccharide) cannot be metabolized, and the sugar pulls
more fluid into the lumen of the bowel. Organic acids and oxygen gas are produced by
bacteria in the lumen, creating watery and acidic stools that contain much flatus.
The most appropriate management of the symptoms described in the vignette is the
administration of a lactose-free diet, which would allow the brush border to repair itself and
once again be able to break down lactose. Once this stabilization has occurred, lactose in the
form of a cow milk formula could be reintroduced. Currently, many studies support
continued feeding through episodes of diarrhea; the protracted symptoms described in the
vignette might have been avoided if appropriate nutrients had been provided earlier in the
course of this illness.
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Gluten-sensitive enteropathy, for which a gluten-free diet would be appropriate,
generally presents in the second half of the first year of life (6 months to 1 year) and can
appear as recurrent diarrhea. However, the triggering food typically is cereal (eg, oatmeal,
barley) or bread (eg, wheat, rye) rather than a cow milk formula. There should be no
symptoms when cow milk is reintroduced. A hypoallergenic diet might lessen the symptoms
seen in the infant in the vignette, but any reintroduction of lactose would recreate them.
Most gastroenteritis in children is caused by viral infections (eg, rotavirus).
Accordingly, administration of antibiotics is not indicated and could be detrimental. For
example, clindamycin and other antibiotics have been implicated in causing
pseudomembranous colitis.
Giardial infections can present with watery diarrhea and sometimes symptomatic
infection may be treated with metronidazole. However, a young infant in the United States is
unlikely to have come in contact a contaminated food or water source.
References:
Committee on Infectious Diseases. Clostridium difficile. In: Report of the Committee on
Infectious Diseases. 24th ed. Elk Grove Village, Ill: American Academy of Pediatrics;
1997:177-178
Committee on Infectious Diseases. Giardia lamblia infections. In: Report of the Committee
on Infectious Diseases. 24th ed. Elk Grove Village, Ill: American Academy of Pediatrics;
1997:210-212
Northrup RS, Flanigan TP. Gastroenteritis. Pediatrics in Review. 1994;15:461-472

Critique 157 Preferred Response: D

[View Question]
Children and infants who have protracted diarrhea may develop alterations in the digestive
function of the brush border of the intestinal mucosa. Intestinal lactase activity is reduced
easily in infants who have diarrhea because it is present in the most superficial layer of this
mucosa; subsequently, the infant's ability to use lactose becomes impaired because of this
secondary lactase deficiency. If the infant continues to be fed milk that contains lactose, the
unabsorbed sugar spills into the distal small bowel and colon, where it is fermented by
bacteria, resulting in the production of hydrogen and carbon dioxide gases. This gas
production leads to cramps, flatulence, and abdominal pain. Additionally, such unabsorbed
sugar can cause an osmotic diarrhea.
There are many causes for acquired or secondary lactase deficiency, including
bacterial enteritis, Giardia lamblia infection, and food allergy. Lactose is the primary
carbohydrate source in human milk and cow milk-based formulas. A child who has
secondary lactase deficiency, such as the one in the vignette, is treated best with a
lactose-free formula, such as lactose-free cow milk or soy formulas, until the lactase activity
of the small intestine normalizes. Evaporated cow milk contains lactose and is
contraindicated in the infant who has secondary lactase deficiency. The prolonged use of oral
rehydration solution is not indicated because the infant needs the additional protein and
calories that formula provides. Goat milk had been used in the past for infants who had milk
protein allergy, but it rarely is used today because other alternative formulas are available.
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Elemental formulas are expensive and should be reserved for infants who have chronic,
protracted diarrhea lasting longer than 2 weeks.
References:
Committee on Nutrition. Formula feeding of term infants. In: Pediatric Nutrition Handbook.
3rd ed. Elk Grove Village, Ill: American Academy of Pediatrics; 1993:17-18
Committee on Nutrition. Practical significance of lactose intolerance in children: supplement.
Pediatrics. 1990;86:643-644
Davis AM, Baker SS. Infant feeding and nutrition. In: Roberts KB, eds. Manual of Clinical
Problems in Pediatrics. 4th ed. Boston, Mass: Little, Brown and Co; 1995:86-89
Lifschitz CH. Carbohydrate needs in preterm and term newborn infants. In: Tsang RC,
Nichols BL, eds. Nutrition During Infancy. Philadelphia, Pa: Hanley & Belfus Inc;
1988:128-130
Montes RG, Perman JA. Carbohydrate malabsorption. In: Rudolph AM, Hoffman JIE,
Rudolph CD, eds. Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange;
1996:1083-1085

Critique 176 Preferred Response: E

[View Question]
Children who have oromotor discoordination often cannot meet the caloric requirements
needed for normal growth. Bolus feedings, if tolerated, are preferable to continuous feedings
because they promote hepatobiliary and pancreatic secretion in response to the feeding
schedule and maintain gastrointestinal absorptive capability. Bolus feedings also stimulate
postprandial gastrointestinal motility. The presence of gastric residuals, malabsorption,
dumping syndrome, aspiration, or persistent regurgitation suggest an intolerance to bolus
feeding, and continuous nasogastric feedings should be tried.
Infants who have congenital heart disease often require nutritional supplementation
because they are receiving insufficient oral intake or they have increased caloric
requirements. The delayed gastric emptying that often is associated with congenital heart
disease results in early satiety or gastroesophageal reflux, which can contribute to
malnourishment. A recent study compared the efficacy of oral feedings of calorically dense
formula (31 kcal/oz), daytime oral feedings plus continuous 12-hour nasogastric feedings,
and 24-hour continuous nasogastric feedings in the management of infants who had
congenital heart disease. The data suggested that only the infants receiving 24-hour
continuous feedings had an increased caloric intake and improved nutritional status. Further,
intensive nutritional support in children who had congenital heart disease allowed for earlier
and safer surgical intervention of their underlying heart defects.
Infants who have gastroesophageal reflux can become malnourished despite oral
nutritional and pharmacologic therapy. After 10 days of continuous nasogastric feedings in
this population, the net caloric intake of infants improved and catch-up growth ensued.
Furthermore, there was a significant reduction in or cessation of vomiting, with many of the
infants remaining free of reflux when oral feedings were initiated. Those infants who failed
to respond to the continuous nasogastric feedings were more likely to have pulmonary
disease, malabsorption syndromes, or static encephalopathy.
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Continuous nasogastric feedings have been effective in controlling the manifestations
of Crohn disease, reversing associated growth failure, and inducing clinical remission.
Patients who have inflammation of the small intestine are more likely to respond to enteral
nutrition than those who have colonic disease; patients who have ulcerative colitis are
unlikely to respond. Although initial studies employed elemental formulas, recent data
suggest that use of a semi-elemental and polymeric diets can produce similar results.
Furthermore, new evidence suggests that continuous nasogastric feeding of elemental
formulas for 6 to 8 weeks is comparable with corticosteroid therapy in producing clinical
remission in children who have Crohn disease. However, after steroids were discontinued and
oral feedings were reinstituted, those who achieved remission using nasogastric feedings
were more likely to suffer relapses than those who received corticosteroids.
Oral or bolus nasogastric feedings may exacerbate diarrhea in children who have
malabsorption syndrome. It is hypothesized that the diarrhea is caused by either large shifts
in luminal fluids that result from the use of hypertonic solutions or stimulation of biliary,
gastric, and pancreatic secretions. In contrast, continuous nasogastric feedings of elemental
formulas in such patients promote nutritional rehabilitation and result in villous atrophy. This
gut atrophy is beneficial in limiting the inflammatory response of the intestine, while the
intraluminal nutrients have a stimulating effect on the intestinal mucosa. Continuous
nasogastric feedings are less likely to cause gastric distension, which also may decrease the
gastrocolic reflex and minimize the frequency of stools.
References:
Belli DC, Seidman E, Bouthillier L, et al. Chronic intermittent elemental diet improves
growth failure in children with Crohn's disease. Gastroenterology. 1988;94:603-610
Ferry GD, Shelby M, Pietro TJ. Clinical response to short-term nasogastric feeding in infants
with gastroesophageal reflux and growth failure. J Pediatr Gastroenterol Nutr. 1983;2:57-61
Giaffer MH, North G, Holdsworth CD. Controlled trial of polymeric versus elemental diet in
treatment of active Crohn's disease. Lancet. 1990;335:816-819
Klein S. Elemental versus polymeric feeding in patients with Crohn's disease--is there really
a winner? Gastroenterology. 1990;99:893-894
Morin CL, Roulet M, Roy CC, Weber A, Lapointe N. Continuous elemental enteral
alimenation in the treatment of children and adolescents with Crohn's disease. JPEN J
Parenter Enteral Nutr. 1982;6:194-199
Morin CL, Roulet M, Roy CC, Weber A. Continuous elemental enteral alimenation in
children with Crohn's disease and growth failure. Gastroenterology. 1980;79:1205-1210
Parathyras AJ, Kassak LA. Tolerance, nutritional adequacy and cost-effectiveness of
continuous drip versus bolus and/or intermittent feeding techniques. Nutritional Support
Services. 1983;3:56-57
Schwarz SM, Gewitz MH, See CC, et al. Enteral nutrition in infants with congenital heart
disease and growth failure. Pediatrics. 1990;86:368-373
Vanderhoof JA, Hofschire PJ, Baluff MA, et al. Continuous enteral feedings. An important
adjunct to the management of complex congenital heart disease. Am J Dis Child.
1982;136:825-827

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Critique 196 Preferred Response: D
[View Question]
Fat absorption in the newborn is less efficient compared with that in the older child and adult.
Because of this, the neonate has a relative steatorrhea, losing up to 20% of ingested fat
through the stool. Malabsorption of the long-chain triglycerides found in infant formula is
due in part to a decrease in both the bile acid pool and pancreatic activity. The presence of
both gastric and lingual lipase can improve fat absorption in the neonate. However, because
the stimulus for lingual lipase is suckling, there is a relative lack of lipase activity in the
preterm infant, which adds to the steatorrhea.
Lipids are the largest single source of energy in both human milk and formula,
providing approximately 50% of the calories. Amino acids from protein sources in both
human milk and formula are well absorbed by infants. Because human milk protein has a
70:30 whey-to-casein ratio compared with an 18:82 ratio for cow milk protein, the amino
acid profile of the breastfed infant differs from that of the formula-fed infant.
Medium-chain triglycerides do not require bile acid activity for absorption because of
their enhanced solubility in water. These fats are hydrolyzed by brush border lipase and
absorbed directly into the portal system. For this reason, formulas specifically designed for
the preterm infant have up to 50% of their total fat as medium-chain triglycerides to decrease
the amount of steatorrhea in these infants. In contrast, mature breast milk contains
approximately 12% of the total fat content as medium-chain triglycerides.
References:
Barness LA, Curran JS. Formula feeding. In: Nelson WE, Behrman RE, Kliegman RM,
Arvin AM, eds. Nelson Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co;
1996:156-163
Byrne WJ. Fat digestion and absorption. In: Taeusch HW, Ballard RA, Avery ME, eds.
Schaffer & Avery's Diseases of the Newborn. 6th ed. Philadelphia, Pa: WB Saunders Co;
1991:660-661
Greer FR. Formulas for the healthy term infant. Pediatrics in Review. 1995;16:107-113
Leleiko NS, Chao C. Fat. In: Rudolph AM, Hoffman JIE, Rudolph CD, eds. Rudolph's
Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange; 1996:1006-1007
Vanderhoof JA, Zach TL, Adrian TE. Gastrointestinal disease. In: Avery GB, Fletcher MA,
MacDonald MG, eds. Neonatology: Pathophysiology and Management of the Newborn.
Philadelphia, Pa: JB Lippincott Co; 1994:605-629
Wilson MH. Feeding the healthy child. In: Oski FA, DeAngelis CD, Feigin RD, McMillan
JA, Warshaw JB, eds. Principles and Practice of Pediatrics. 2nd ed. Philadelphia, Pa: JB
Lippincott Co; 1994:601-603

Critique 216 Preferred Response: D

[View Question]
Of all of the options provided in the vignette, the most likely maternal reason for
unsuccessful breastfeeding is inverted nipples. If the nipples are inverted, the use of milk
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cups as early as the third month of pregnancy can be helpful. If the nipples are retracted, the
mother may benefit from daily manual breast pump traction during the last few weeks of
pregnancy.
Fibrocystic breast disease should not interfere with lactation. However, prior breast
surgery (eg, mammoplasty for breast augmentation or reduction) may result in the inability to
breastfeed if the ductal system has been disrupted. Treatment of contact dermatitis by
eliminating the offending agent and candidiasis with the appropriate antifungal medication
should not interrupt breastfeeding.
In mastitis, plugging of the mammary duct can lead to milk stasis and occasionally
infection. Treatment consists of antibiotic therapy and pain relievers. Nursing is encouraged
because it can help relieve the pressure from congestion. Other factors that may lead to
unsuccessful breastfeeding are sore nipples, breast engorgement, maternal fatigue, and stress.
Although the preterm infant may not be able to nurse at the breast initially, manual
expression of the milk will allow the infant to be fed human milk. With appropriate maternal
encouragement and counseling, the infant likely will be able to enjoy the benefits of human
milk obtained directly from the breast as he or she matures.
References:
D'Harlingue AE, Byrne WJ. Feeding healthy term infants. In: Taeusch HW, Ballard RA,
Avery ME, eds. Schaffer & Avery's Diseases of the Newborn. 6th ed. Philadelphia, Pa: WB
Saunders Co; 1991:712-713
Fletcher AB. Nutrition. In: Avery GB, Fletcher MA, MacDonald MG, eds. Neonatology:
Pathophysiology and Management of the Newborn. Philadelphia, Pa: JB Lippincott Co;
1994:330-356
Needlman RD. Breast-feeding. In: Nelson WE, Behrman RE, Kliegman RM, Arvin AM, eds.
Nelson Textbook of Pediatrics. 15th ed. Philadelphia, Pa: WB Saunders Co; 1996:152-156
Overby KJ. Counseling and anticipatory guidance. In: Rudolph AM, Hoffman JIE, Rudolph
CD, eds. Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange; 1996:19-29
Wilson MH. Human milk feeding. In: Oski FA, DeAngelis CD, Feigin RD, McMillan JA,
Warshaw JB, eds. Principles and Practice of Pediatrics. 2nd ed. Philadelphia, Pa: JB
Lippincott Co; 1994:589-605

Critique 236 Preferred Response: D

[View Question]
The normal values (mean ± 2 standard deviations) of hemoglobin and hematocrit obtained
from the cord blood of term infants or capillary samples obtained on days 1 to 3 of life are as
shown in the following table:
The average capillary hematocrit value for a term infant during the first three days of
life is closest to 56%. Hemoglobin concentrations and hematocrit remain fairly stable for at
least the first 1 to 3 weeks of life, then begin to fall steadily at a rate of almost 1 g/dL of
hemoglobin per week until a nadir is reached at 7 to 9 weeks of life.
Hemoglobin and hematocrit are higher in the neonatal period than at any other time of
life. The fetus is relatively hypoxemic, and a higher in utero hemoglobin concentration
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provides critical additional oxygen capacity. In childhood, clinicians are most interested in
the lower end of the range of normal values because anemia is quite common, whereas
clinically significant polycythemia is exceedingly rare. In the neonate, however,
polycythemia is not only common, but it can be symptomatic. Thus, it is important to know
both the lower and upper limits of normal for hemoglobin in the neonate.
When interpreting the normal hematologic range, it is critical to consider the site of
sampling. Other than those from cord blood, most samples from neonates are obtained from
capillary blood. The hemoglobin concentration and hematocrit of capillary samples virtually
are always higher than venous samples. This difference, which can be 20% or more, is
greatest in the most immature, acidotic, or hypotensive infants. Adequate warming of the heel
prior to sampling appears to bring the capillary values closer to venous values, but this may
be less helpful in infants who have polycythemia or in those who are extremely preterm.
References:
Mentzer WC. Blood and blood-forming tissues. In: Rudolph AM, Hoffman JIE, Rudolph CD,
eds. Rudolph's Pediatrics. 20th ed. Stamford, Conn: Appleton & Lange; 1996:1167-1172
Oski FA. The erythrocyte and its disorders. In: Nathan DG, Oski FA, eds. Hematology of
Infancy and Childhood. 4th ed. Philadelphia, Pa: WB Saunders Co: 1993:26-31

Critique 253 Preferred Response: E

[View Question]
Enteral feeding is a safe and effective method of providing nutrition support if the formula
used, the method of infusion, and the site where the infusion is introduced are monitored
carefully. Vomiting occurs in approximately 20% of adults receiving nasogastric feedings.
Gastroesophageal reflux, increased intracranial pressure, medications, and malposition of the
nasogastric tube cause the majority of cases of this complication. Vomiting with aspiration is
the most severe complication associated with enteral feedings. Severe aspiration occurs in
1% of patients who vomit following enteral feeding.
Diarrhea occurs in 10% to 30% of children receiving nasogastric feedings but rarely
results in dehydration. Its frequency depends on the concomitant administration of antibiotics
or other medications, malnutrition, osmolarity of the formula, and the presence of
hypoalbuminemia. In patients receiving only elemental diets, diarrhea is uncommon
regardless of the composition or osmolarity of the formula used. Constipation may occur in a
patient receiving an elemental diet and can be controlled by adding fiber to the formula.
Metabolic abnormalities may be present in malnourished patients who have diabetes
mellitus or enteric, hepatic, or renal diseases. Water deficiency may occur in those receiving
hyperosmolar and hypercaloric formulas that contain little free water. Patients who develop
fever, vomiting, or diarrhea and those living in warmer climates need to have their fluid
status monitored closely to avoid dehydration.
Mechanical obstruction of the nasogastric tube presents a major difficulty in patients
receiving thick solutions or nasogastric medications. Allergic reactions to the polyvinyl or
silicone nasogastric tubes are uncommon. Insertion-related complications of nasogastric
feeding include trauma and bleeding from the nose or upper gastrointestinal tract; perforation
of the cribriform plate or esophagus; and respiratory distress resulting from coiling of the
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tube in the nasopharynx, aspiration pneumonitis, or vomiting. However, gastric perforation
and gastritis are rare. Migration of the nasogastric tube, sinusitis, and otitis media are
potential complications of long-term use of tube feedings.
References:
Jones BJ, Lees R, Andrews J, Frost P, Silk DB. Comparison of an elemental and polymeric
enteral diet in patients with normal gastrointestinal function. Gut. 1983;24:78-84
Keohane PP, Attrill H, Love M, Frost P, Silk DB. Relation between osmolality of diet and
gastrointestinal side effects in enteral nutrition. Br Med J (Clin Res Ed). 1984;288:678-680
Mullan H, Roubenoff RA, Roubenoff R. Risk of pulmonary aspiration among patients
receiving enteral nutrition support. JPEN J Parenter Enteral Nutr. 1992;16:160-164
Wilson SE. Pediatric enteral feeding. In: Grand RJ, Sutphen JL, Dietz WH Jr, eds. Pediatric
Nutrition: Theory and Practice. Boston, Mass: Butterworths; 1987:771-786

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