STATE ESTABLISHMENT "DNIPROPETROVSK MEDICAL ACADEMY OF HEALTH MINISTRY OF UKRAINE" PEDIATRICS DEPARTMENT 2 “Confirmed;” METHODICAL INSTRUCTIONS FOR STUDENTS’ SELF-WORK WHILE PREPARING FOR PRACTICAL LESSONS Educational discipline __| pediatrics | module No 2 Substantial module Ne [10 | Theme of the lesson DEFICIENCY ANEMIAS IN CHILDREN Course 5 (Faculty [TW intemational Dnipro, 2018.Iron, protein. min deficiency anemia in children 1. Actuality of the topic: Anemia is one of the most widespread forms of hematological pathology in children. Over 50% of childish population are suffering Fe deficiency anemia. Starting at early age anemia takes relapsing course and causes formation of heavy complications. Anemia at early age should be considered as a risk factor which influences acute respiratory diseases, pneumonia, rachitic diseases. These diseases occur 3-5 times more often in children with anemia than in healthy children, Correct and timely determination and treatment of anemia prevents development of heavy complications and consequences. These facts explain actuality of the present topic. 2. Certain purposes: A.A student should know: Definition of term “anemia” Classification of deficiency anemias in children Etiopathogenetical peculiarities of deficiency anemias at early age Importance of development factors in different forms of anemias Causes of Fe deficiency development in a child’s body Causes of vitamin deficiency (vit.Bj2) development, folic acid, proteins in a child’s body 7. Pathogenesis of deficiency anemias in children 8. Laboratory signs of Fe, vitamin, protein deficiency anemias 9. Differential diagnosis of various deficiency anemias 10. Principles of therapy of deficiency anemias in children 11. Peculiarities of administration Fe-therapy in children of early age 12. Principles of prophylaxis of deficiency anemias at child’s age 13, Outcomes of different anemias in children PAB LE B. A student should be able: 1. To develop a scheme of diagnostic search in cases of anemia 2. To take patient’s blood disease anamnesis 3. To carry out patient’s objective study 4, To estimate laboratory data. To choose among analyses those which testify to anemia 5. To determine clinical diagnosis criteria in cases of different anemia forms 6. To represent detailed clinical diagnosis according to the classification 7. To carry out differentiated diagnosis of anemia and other blood diseases in children 8, To administer adequate treatment taking into consideration the form of the disease 9. To carry the disease prophylaxis 10. To use deontological principles while taking anamnesis, objective patient’s check 3. Tasks for self-study work while preparing for the lesson. 3.1. List of basic terms, medicines, characteristics which a student should master while preparing for the lesson: Term Definition Fe deficiency anemia | Decrease of hemoglobin levels in circulating blood due to Fe deficiency in the bodyAnemic syndrome Syderopoenie syndrome Degree of severity of IDA Color index Serum Fe General Fe-binding serum ability ‘Transferrin saturation index Day dose of elementary Fe for per os administration is (according to WHO): Formula for calculation of elementary Fe course dose in case of per os administration: Course dose of Fe- containing medicine (CDM): ‘Number of injections throughout the course: Syderoacrestic anemia Megaloblastic anemia | | Folic-deficiency anemia (FDA) Bi2— deficiency anemia (Bi-DA) Symptoms: dryness, fatigue decrease of appetite, asthenia, skin pallor, tachypnea, tachycardia, weakening of heart sounds, abnormal systolic sound, in heavy cases — delay in growth and mental activity Symptoms: dryness, skin pigmentation, hyper-keratosis of knee and cubital areas, dystrophy of hair, nails, caries without particular symptoms, distortion of smell and taste, angular stomatitis, atrophic glossitis, pacctpofictna digestion disorders, blue scleras. mild -Hb 110-91 g/l moderate -Hb 90-71 g/l severe -Hb 70-51 g/l very severe - Hb 50 g/l and less Reveals hemoglobin saturation of erythrocyte. Norm 0.85-1.5 Conditionally responses to amount of Fe bound with transferrin. Norm in infants: 5.0-19.0 mkmol/I > month: 10.6-33.6 mkmol/ Characterizes general amount of Fe which can be bound with serum transferrin. Norm 40.6-62.5 Specific gravity of serum Fe from all serum Fe-binding ability ‘Norm ~not less than 17%. For children — younger than 3 years old - 3-5 mg/kg/day ~4-7 years old - 50-70 mg/day —over 7 years old - 100 mg/day BW( (78-0.35( Hb), where BW — body weight (kg) Hb ~ child's hemoglobin (g/l) CDM = CDF : FCM, where CDF — course dose of Fe (mg); FCM-Fe content (mg) in 1 ml of medicine CDM: DDM, CDM — course does of medicine (ml) DDM - daily dose of medicine (ml) Anemia caused by enzyme disorders in hemoglobin synthesis and defects of Fe inclusion in heme at high Fe level in serum Group of anemias with ineffective erythroporesis characterized by disorders in maturing and morphological changes in erythrocytes, Can be caused by deficiency of folic acid in food Can be caused by deficiency of vitamin Brzin food3.2, Theoretical questions to the lesson: 1. Definition of term “anemia” 2. Classification of deficiency anemias in children 3. Etiopathogenetical peculiarities of deficiency anemias at early age 4, Importance of development factors in different forms of anemias: ‘© deficiency of Fe and other microelements * deficiency in B-group vitamins * deficiency of folic acid * protein deficiency * congenital and genetic factors # acute and chronic pathologies 5. Clinical symptoms in various forms of deficiency anemias in children 6. Patient's check-up for anemia ‘clarification of complaints revealing typical data from anamnesis ‘© objective patient’s check-up 7. Importance of additional check-up methods for diagnosing anemia 8. Principles of anemia therapy in children 9, Medicines with Fe in therapy 10. Prophylaxis of deficiency conditions in children 11, Outcomes of different anemias 3.3. Practical skills (tasks) mastering during practical lesson: 1. To collect complaints, case history and personal (life) history 2. To inspect the child consistently 3. To reveal early symptoms of deficient anemias at children 4, To evaluate the condition of the child and available clinical symptoms. 5. To evaluate the results of the additional methods of investigation 6. To make the clinical diagnosis according to classification, 7. To make the treatment plan 8. To make recommendations of dispensary supervision. 3. Maintenance of the subject: Iron deficiency anemia (IDA) ICD-X Code: D 50 1. Definition Iron deficiency anemia (IDA) - a pathological condition which is characterized by decrease in the content of hemoglobin owing to the deficiency of iron in the organism as the result of the disorders of its income, assimilation or pathological losses. WHO criteria (1973) - the lower level of hemoglobin of capillary blood at children younger than 6 years - 110 g/l, older than 6 years - 120 g/l. 2. The causes of IDA at children: - insufficient initial level of iron in the organism (disorders of uterine placental circulation, fetomaternal and fetoplatsental bleedings, syndrome of fetal transfusion atmultiple pregnancy, prematurity, severe and prolonged deficiency of iron at the pregnant ‘woman, early or late ligating of an umbilical cord, intranatal bleeding owing to traumatic obstetric interventions or anomaly of the placental and umbilical cord vessels development) - increased requirement of iron (prematurely born, children with a big weight at the birth, with lymphatic type of the constitution, children of the second half of the year of life). - insufficient content of iron in food (early artificial feeding with cow or goat milk, flour, dairy or vegetarian food, an unbalanced diet in which there is insufficient content of meat products) = increased losses of iron owing to bleeding of various etiology, disorders of intestinal absorption (chronic intestinal diseases, syndrome of malabsorbtion), considerable and prolonged uterine bleedings. = disorders of iron exchange (prepubertal and a pubertal hormonal imbalance) orders of iron transport and utilization (decreased level of transferring or its absence, cenzimopathy, autoimmune processes) - insufficient resorption of iron in the gastrointestinal tract (after resection of the stomach and gasterectomy). 3.. Stages of development of IDA (WHO, 1977) = prelatent (exhaustion of tissue iron reserves; blood parameters are within normal limits; clinical manifestations are absent). = latent (deficiency of iron in tissues and reduction of its transport fund; blood parameters are within normal limits; clinical manifestations are caused by trophic disorders which develop owing to decrease in activity of iron-containing enzymes and are manifested by sideropenic syndrome - epithelial changes of skin, nails, hair, mucous membranes, distortion of the taste, scent, disorders of intestinal absorption and asteno-autonomic functions, decrease in local immunity). - iron deficiency anemia (more expressed exhaustion of tissue reserves of iron and mechanisms of compensation of its deficiency; changes in blood analysis depending on the severity of the process; clinical manifestations in the form of a sideropeni syndrome and general anemic symptoms which are caused by an anemic hypoxia - tachycardia, a muffled heart tones, systolic murmur, dyspnea on exertion, pallor of skin and mucous membranes, arterial hypotonia, increase of asteno-neurotic disorders). Severety of an anemic hypoxia depends not only upon hemoglobin level, but also upon the speed of development of anemia and upon compensatory opportunities of an organism, In severe cases the syndrome of metabolic intoxication in the form of decreased memory, subfebrile fever, headache, fatigue, hepatoloenal syndrome, and etc. develops. Deficiency of iron causes decreased immunity, a delay of psychomotor and physical development of children. Degrees of severity of IDA by the level of hemoglobin: light - Hb of 110-91 g/l moderate - Hb of 90-71 g/l severe - Hb 70-51 g/l very severe — Hb less than 50 g/l 4. Laboratory criteria of diagnostics of ID, Complete blood count: Level of hemoglobin, erythrocytes morphological changes of erythrocytes color indexmean diameter of erythrocytes mean concentration of hemoglobin in an erythrocyte (MCHC) mean volume of erythrocytes (MCV) level of reticulocytes biochemical analysis: concentration of iron and ferritin general iron-binding capacity of blood latent iron-binding capacity of blood coefficient of transferrin saturation by iron 5. Basic principles of treatment ~ elimination of ethyological factors - balanced nutrition (for infants — breastfeeding, adapted formulas enriched with iron, timely introduction of solids, meat, especially veal, subptoducts, buckwheat and oat grain, fruits and vegetables, cheese; reduction of phytates, phosphates, tannin, calcium intake which worsen iron absorption). - pathogenetic treatment by iron preparations mainly in the form of drops, syrups, tablets. Indications to the parenteral administration of iron preparations: at syndrome of disordered intestinal absorption and after a profound resection of the small intestines, not specific ulcerative colitis, severe chronic enterocolitis andd dysbiosis, intolerance of oral iron preparations, severe degree of anemia. ~ preventive measures to prevent its recurrence Correction of iron deficiency at light anemia is carried out mainly by balanced diet, sufficient stay of the child in the open air. Iron preparations should not be administered at the level of hemoglobin of 100 g/l and above. Daily therapeutic doses of oral iron preparations at moderate and severe IDA. till 3 years - 3-5 mg/kg/day of elementary iron from 3 to 7 years - 50-70 mg/day of elementary iron older than 7 years — up to 100 mg/day of elementary iron Control of efficiency of the prescribed dose is performed by the definition of the increase of the reticulocyte level at 10-14 days of treatment. Iron therapy is carried out until the level of hemoglobin normalizes with further reduction of a dose. Treatment duration - 6 month, for preterms - 2 years for replenishment of iron reserves in the organism. Older children have a supported dose of 3-6 months, girls of pubertal age — intermittently within a year - every week after menses. It is prudent to administer preparations of trivalent iron owing to their optimum absorption and lack of side effects. ‘At children of younger age IDA has mainly alimentary causes and often is associated with multiple protein and vitamin deficiencies, that’s why administration of vitamin C, B1, B6, folic acid, correction of the contents in the diet of proteins should be performed ‘As 50 - 100% of prematurely bom children have late anemia, since 20-25 days of life at gestational age of 27-32 weeks, weight of 800-1600 g, (if of hemoglobin level is 110 g/l and less, erythrocytes level is less than 3,0x10'"/, reticulocytes less than 10%), there should be prescribed iron preparations (3-5 mg/kg/day), sufficient protein intake (3-3,5 g/kg/day) and erythropoietin subcutaneously 250 Urkg/day three times per week for 2-4 weeks, with vitamin E (10-20 mg/kg/day) - 5 times for a week, with its gradual decrease to 3 times, it is appointed to children with a severe intranatal or postnatal infection, and also to children with the low retyculocyte response to the therapy.Parenteral iron preparations have to be used only by special indications, owing to the risk ‘development of local and system adverse reactions. The daily dose of elementary iron for parenteral administration: for children of 1-12 months — up to 25 mg/day 1-3 years - 25-40 mg/day older than 3 years - 40-50 mg/day Course dose of elementary iron count on the formula: W ((78-0,35 (Hb), where W- body weight (kg) Hb - hemoglobin of the child (g/1) Course dose of iron-containing preparation - CD: Cl, where CD ~a course dose of iron (mg); CI- contents of iron (mg) in 1 ml of the preparation Course quantity of injections - CDP:DDP, where CDP-course dose of a preparation (ml); DDP - a daily dose of a preparation (ml) Contraindications to iron-therapy: aplastic and haemolytic anemia, hemochromatoses, hemosiderosis, sideroachrestic anemia, talassemiya, other types of anemias which aren't caused by the deficiency of iron in the organism. Hemotransfusions are carried out only on vital indicators when there is acute massive blood loss. Packet red cells or washed erythrocytes should be used. 6. Prevention Antenatal: to women from the 2nd half of pregnancy prescribe iron preparations or the polyvitamins enriched with iron. At repeated or multiple pregnancy an obligatory administration of iron drugs throughout the 2nd and 3rd trimester. Postnatal prevention for children from high risk group of development of IDA. This group form: + all prematurely born children + children who were born from multiple pregnancy and at the complicated caurse of the second half of pregnancy (gestoses, fetoplatsental insufficiency, complication of chronic diseases) + children with intestinal dysbiosis, food allergy * children who are bottle-fed + children who have accelerated growth Regular carrying out diagnostics of possible development of IDA and is supposed, if it is confirmed preventive doses of iron preparations of iron (0,5-1 mg/kg/day) for 3-6 month should be prescribed, 7. Dispensary supervision After normalization of blood parameters complete blood count is carried out once a month for the first year, then - quarterly for the next 3 years. Megaloblastic anemias (MA). ‘The group of anemias with inefficient erithropoesis that is characterized by disorder of maturing and change of morphology of erythrocytes. In the blood swab - anysocytosis, poikilocytosis, hypersegmentation of neutrophils, primary or secondary deficiencies of folic acid and cyanocobalamine (B12)Folie deficiency anemia (FDA). ICD-X D52 code More often is observed at preterms. IDA develops at children who eat exclusively goat milk. Causes of IDA: congenital disorders of adsorption and exchange of folates, acquired malabsorbtion, increased requirements in folates at severe preterm infants, at haemolytic anemias and others. In 2-3 weeks after folic deficiency its level in serum decreases, in 3 months ~ megaloblastic changes in marrow and peripheral blood, in urine increase of forminin-glutamine acid (a sign of folate and B12 deficiency at MA). Clinical manifestations: deeply prematurely born children in case of folate deficiency at the age of 3-6 months have MA, weakness, anorexia, glossitis, chronic diarrhea, increased bleeding and bacterial infections. Treatment: folic acid is administered orally in a dose - 2-5 mg/day, duration — not less than 3 ‘weeks. In the absence of effect at MA it is necessary to think of deficiency of vitamin B12, at malabsorption — parenteral administration. Prevention: to deeply prematurely born children since 2 months, to children from risk group to receive folic acid every day in a dose 0,2-0,5 mg. B12 - deficiency anemia (B12 DA). ICD-X D51 code Can be a consequence of deficiency of vitamin in food (strict vegetarianism), hereditary disorders (congenital deficiencies of sorption ~ Kast's internal factor, transport and metabolism of vitamin B12), acquired defects of absorption, etc. Clinical manifestations: V12-DA can mnifest at children since 6 months at congenital lack of a Kastl factor of. Older children have symptoms of MA signs (pallor, icterous sclera and , dryness of skin, fragility of hair and nails, weakness, decreased appetite with special disgust for meat, etc.), glossitis with an atrophy of papillas (the varnished language), pain in the tongue with aphtous changes, nervous system disorders from owing to dorsolateral degenerate changes in the spinal cord (ataxy, paresteziya, hyporeflection, clonuses, pathological reflexes, feeling of wadded feet, hallucinations, dream, signs of heart failure, the diarrhea, hepatolienal syndrome). In peripheral blood - MA (erythrocytes with Zholli's bodies, Kebot’s rings, megalocytes, megaloblasts), neutropenia, thrombocytopenia. In urine - increase of metilmalone acid (a differintial-diagnostic sign of IDA). Treatment: parenteral administration of vitamin B12 in a dose of 200-500 mcg every day, at neurologic manifestations a dose increase to 1 mg. At hereditary forms of V12-DA after resolution of acute clinical manifestations it is recommended to administer cyanocobalamine 1 mg into 3 months. Additional materials for the self-control Clinical cases Case 1 A 3-year-old Caucasian gir] is brought to the community clinic of a rural town because of cough and fever. She looks extremely pale, and a hemoglobin level by finger stick is 1.12 mmol/L (1.8 g/dL). There is no history of trauma, pica, hematemesis, hematochezia, melena, jaundice, or tea-colored urine. The only medication she has taken recently is ibuprofen. She is transferred to the pediatric ward of the regional hospital. On physical examination, her weight is 10.9 kg, temperature is 39.2°C (102.6°F), pulse is 142 beats/min, and blood pressure is 117/62 mm Hg, She is alert and cooperative, but appears ill, is in mild respiratory distress, and is extremely pale, with no pink color in the nail beds. She has no jaundice or lymphadenopathy. She is breathing at 66 breaths/min with mildretractions; inspiratory and expiratory crackles are audible over the left lung base. An $3 gallop rhythm is noted. Her abdomen is slightly distended. The liver edge is palpable 2 to 3 ‘cm below the costal margin, but the span is normal; the spleen is not palpable. There is mild pretibial edema. Her hemoglobin level is 0.87 mmol/L (1.4 g/dL), hematocrit is 0.054 (5.4%), platelet count is 242 x 10°/L (242.x 10°/meL); and leukocyte count is 24 x 10°/L (24 x 10°/meL.), with 45% neutrophils, 31% band forms, 22% lymphocytes, and 2% metamyelocytes. The mean corpuscular volume (MCV) is 50.5 fL (normal, 82 to 98 fL). The blood smear, reviewed by the pathologist, does not show any blasts. The dietary history revealed that since late infancy the patient, who is the youngest of four children, has continued to drink six 8-oz bottles of cow milk per day, with nearly no intake of solid foods. Questions What is the presumptive diagnosis ? How to confirm it? What are the predisposing factors? Write down confirmation of the diagnosis. How to treat this condition ? veers Case 2 A.22 month old boy presents to your office with a chief complaint of pallor. A visiting relative who has not seen the child for 5 months told his mother that the boy appears pale. ‘The mother brings him in for a checkup even though she notices no change in his coloring (he has always been fair skinned). On review of symptoms you find that he is an active toddler, with no recent fatigue, exercise intolerance, or increase in sleeping. He has had no blood in his diapers and no black or tarry stools. He is a picky eater, taking small amounts of chicken, pork and some vegetables, but loves milk and drinks six to eight bottles of whole milk per day. Family history reveals a distant aunt who had anemia when she was pregnant but which subsequently resolved. There is no history of splenectomy, gall stones at an early age, or other anemia in the family. Exam: VS: T 37.5, BP 90/52, P 145, RR 16, Height 85.5, Weight 13.2 kg. General appearance: He is a pale appearing, active toddler, holding a bottle, tearing and eating paper from your exam table. Eyes: No scleral icterus. Pale conjunctiva. Mouth: Dental caries. Chest: Clear. Heart: Mild tachycardia as above, grade II/VI systolic ejection murmur heard best over the upper left sternal border. Abdomen: No hepatosplenomegaly. Rectal: Dark brown, soft stool, negative for occult blood. CBC: WBC 6,100, Hgb 6.2 g/dl, Het 19.8%, Plt $89,000, MCV 54 fL, RDW 17%. Reticulocyte count is 1.8%. The lab reports microcytosis, hypochromia, mild anisocytosis and polychromasia, There is no basophilic stippling. Questions ‘What is the definitive diagnosis? What are the predisposing factors? Write down confirmation of the diagnosis. How this condition should be corrected? Bene Case 3 Presentation A.17 year old non-vegetarian Asian female student presented with a three year history of increasing lethargy and shortness of breath during exercise. On examination she was clinically anaemic but had no other physical signs. Haematological investigations, including a blood film, were performed. Her haemoglobin was 85 g/l, mean cell volume was 79 fl, mean cell haemoglobin was 25 pg, haematocrit was 29%, white blood cell count was 5.0x10"/, differential cell count was normal, and platelets were 550x10"/.Questions 1. What abnormalities can be seen in the blood film? 2. Evaluate complete blood count. 3. What type of anaemia is it? 4, What is the likeliest cause? 5. What are the principles of treatment? B. Tests Question 1. All of the following statements regarding iron deficiency are true Except: A. Because absorption of dietary iron is assumed to be about 10%, a diet containing 80-100 mg of iron daily is necessary for optimal nutrition B. Intense exercise conditioning may result in iron depletion in adolescent girls C. C.lron deficiency may have effects on neurologic and intellectual function D. The level of serum ferritin provides a relatively accurate estimate of body iron stores in the absence of inflammatory disease E. The red cell distribution width (RDW) is elevated in iron deficiency but not in and thalassemia trait Answer A. Question 2. The breast-fed infant of a mother who is a strict vegan may experience deficiencyof which of the following vitamins if the mother is not receiving supplements of the vitamin? AK B.B6 CBI2 D. Folate EBiotin Answer C. Explanation: A strict vegan diet contains no eggs, meat, or milk products and is thus deficient in vitamin B12. 10Question 3.The best source of iron for 1-mo-old infants is: A lron-fortified cereals B. Yellow vegetables C. Fruits D. Breast milk E. 2% lowfat cow's milk Answer D. Explanation: Although breast milk contains relatively less iron by weight, the iron is more bioavailable than the iron in cereals. Fruits, yellow vegetables, and cow's milk are poor sources of iron. Question 4. All of the following are clinical manifestations of kwashiorkor except: A. The presence of edema B. Rash in sun-exposed areas C. Hypochromotrichia D. Muscle weakness E. An increased susceptibility to infection Answer B. Explanation: The rash of kwashiorkor is in areas of irritation. Sunexposed dermatitis is typical of pellagra. Question 5.All of the following are laboratory manifestations of kwashiorkor except: A. Persistent ketonuria B. Hypoalbuminemi C. Hypoglycemia D, Potassium deficiency E, Low serum amylase levels Answer A. Explanation: Ketonuria is present early but does not persist into the later stages, Question 6. An exclusively breast-fed infant with poor routine care is switched at 6 months of age to whole milk and table foods. Screening laboratories at 9 months of age demonstrate the hemoglobin and hematocrit to be 8 mg/dL and 25%, respectively, and the lead level to be less than 2 g/dL. A follow-up complete blood count (CBC) 2 weeks later shows the hemoglobin to be at 7.8 mg/dL, the hematocrit 25%, the mean corpuscular volume (MCV) 62%, and the platelet count to be 750,000/mm3. Which of the following would be the next step in the management of this child? A. Order a hemoglobin electrophoresis. B. Obtain a bone marrow aspiration. C. Initiate iron supplementation, D. Refer to a pediatric hematologist. E. Initiate soybean-based formula. Answer C. The child in the question likely did not get iron (or vitamin D) supplementation in the first 6 months of life while exclusively breastfeeding and was switched to whole milk (low in iron) and to table foods (not supplemented with iron as are baby foods) at too young an age. All of the laboratory data are consistent with iron deficiency anemia; iron supplementation in this child with a resultant brisk erythrocyte response is both diagnostic and therapeutic, Failure of the child to respond to the iron therapy would require further evaluation. rtQuestion 7. You are called to the bedside of a mother who just delivered a healthy term infant and has a question regarding her infant’s nutrition. The mother was fed goat’s milk as a child and wants to do the same for her infant. Under which of the following conditions is goat's milk acceptable as infant nutrition? A. Goat's milk proteins are hydrolyzed before feeds. B. Infants are provided supplemental vitamins and minerals. C. Goat’s milk is freshly obtained from goats. D. Infants of mothers with milk intolerance should preferentially receive goat’s milk. E. Goat's milk is diluted with water. Answer B. Infants drinking goat's milk must have nutritional supplementation with vitamin B12, folate, and iron. Several goat's milk-based formulas including these nutrients are available. Fresh, unpasteurized goat's milk can contain Brucella ovis and cause brucellosis. Diluting milk will only serve to dilute the caloric content. Question 8. You receive the results of a CBC you performed in your clinic on a pallorous 9- month-old boy. Other than pallor, no historical or physical examination concerns were noted during the patient's visit. The laboratory technician reports a hemoglobin of 8.6 g/dL, an MCV of 105 fL, and platelet count of 98,000/mm3. You are also told that the white blood cell count is 8500/mm3 and the differential reveals 47% neutrophils and 42% lymphocytes, and that no atypical lymphocytes are seen. Which of the following is the most appropriate next step in this child’s care? ‘A. Measurement of serum iron and total iron binding capacity levels. B. Initiate oral iron supplementation. C. Measurement of vitamin B12 and folate levels. D. Begin oral vitamin B12 and folate supplementation. E, Obtain a STAT referral to pediatric hematologist. Answer C. This infant has hematologic parameters consistent with macrocytic anemia. The mild thrombocytopenia reported is periodically seen in patients with vitamin B12 deficiency, and is thought to be related to impaired DNA synthesis and ineffective thrombopoiesis. The results reported are not typical for iron deficiency and neither an iron panel nor iron supplementation is warranted. At this point, your workup should include checking folate and B12 levels; supplementation of these compounds is not yet justified. Myelodysplasia or leukemia is in the differential, but is probably less likely with anormal white blood cell count and differential (no atypical cells); referral to Pediatric Hematology may ultimately be required, but some preliminary data can be gathered first. Question 9. The parents of a previously healthy 3-year-old girl bring the child to your office because she is complaining that her tongue hurts. The parents also report she has appeared weak and listless over the last several months, and has not been eating well. Recently she has exhibited trouble walking. The family usually eats a regular diet, including meats and vegetables. On physical examination, her tongue is smooth, red, and tender. She is pale and tachycardic. Her complete blood count reveals a macrocytic anemia. Which of the following is the most likely diagnosis in this child? A. Folate deficiency B. Iron deficiency C. Vitamin D deficiency D. Zine deficiency E, Vitamin B12 deficiency 12Answer E. This is the typical presentation for juvenile pernicious anemia, a rare autosomal recessive condition in which the child is not able to secrete intrinsic factor and cannot absorb vitamin B12. Supplies of vitamin B12 passed to the fetus from the mother typically are sufficient for at least the first 1 to 2 years of life. A deficiency in transcobalamin results in megaloblastic anemia in infancy because transcobalamin is required for B12 transport and utilization; therefore, vitamin B12 provided by the mother cannot be used effectively. Question 10. You are working at a Native American clinic in Alaska. A 16-year-old adolescent female comes to your office for an evaluation of lethargy. Her father notes that recently she has looked pale. She eats a regular diet and has no significant past medical history. Her menses are regular and have not been excessive. During the last few years, she has helped her mother in the family seafood restaurant after school, but is increasingly tired and unable to complete all of her work. Her complete blood count reveals a ‘megaloblastic anemia. Which of the following is the next appropriate study? A. Folate level B. Stool for rotavirus C. Iron level D. Stool for ova and parasites E, Transcobalamin level ‘Answer D. The fish tapeworm Diphyllobothrium latum uses vitamin B12 for growth and egg production; as many as one million eggs per day may be produced. The parasite also inactivates the vitamin B12-intrinsic factor complex, inhibiting absorption in the terminal ileum. The fish tapeworm is the longest tapeworm to infect humans, sometimes growing to more than 10 m in length. Most infestations are asymptomatic, with megaloblastic anemia occurring in 2% to 9% of tapeworm infections. Risk factors include eating raw or undercooked fish. In North America, it is most commonly seen in the northern United States, Alaska, and Canada. Eggs have a unique morphology and are easily found in stool samples. Question 11. 10-year-old boy with acute blood loss has acute falling of blood pressure, expressed lethargy, thirst. Skin is pale, covered with sticky cold sweat; thready pulse, 132/min; breathing is superficial, tahypnea, What causes such condition?: A Hypovolemia B Hypoxemia C Hyperkalemia D Acidosis. E Hypothermia, Question 12. The child is 8 month old. Throughout last month has insufficient weight gain, decreased appetite, increasing weakness, has fragile and cross-section nails, dry skin, angular stomatitis, atrophy of tongue papillas. Complete blood count: decresed erythrocytes - 3.0x10 12/l, hemoglobin - 68 g/l. What is the most probable genesis of this anemia? A Deficiency B Posthemorthagic C Haemolytic D Infectious-toxie E Hypoplastic Question 13. 5-month-old child was born prematurely, in the newborn period and was not ill. 1BLiterature 1, Nelson Textbook of Pediatries. - 18th ed. / Ed. by R. Kliegman et al.-Philadelphia: Saunders Co, 2007.- 3146 p. 2. Pediatry. Guidance Aid / 3a pen. O.B. Tarxka; 0.11. Bismupxa, T.1. JIytaii—K. : Mesununa, 2007 . ~ 158 c. 3. Current Pediatric Diagnosis & Treatment (CPDT). - 18th ed./ Ed. By W.W.Hay et al. - The McGraw-Hill Companies. ~ 2006. 4, Current pediatric therapy -18th ed. / Ed. by F.D.Burg et al. - Elsevier Inc. ~ 2007. 5. Nelson Essentials of Pediatrics -Sth ed. / Ed. by B.S.Siegel, J.J.Siegel. - Elsevier Ine. ~ 2007. 6. ABC of Clinical Haematology - 2nd ed. D. Provan. - BMJ Books. ~ 2003. 7. Hematology. Basic Principles and Practice - 4th ed. / Edited by R.Hoffman et al. - Elsevier Inc. — 2005. 8. Practical Algorithms in Pediatric Hematology and Oncology / Edited by R. H. Sills. Karger AG, P.O. - 2003.