儿童贫血全英文ppt课件

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1、Anemia in childhood(小儿贫血)To understand features of hematopoiesis and blood in children.To comprehend clinical features,diagnosis and therapy of anemia.To understand the definition,grade division and classification of anemia in children.To master etiology,pathogeny,diagnosis,therapy and prevention of

2、 nutritional iron deficiency anemia and nutritional megaloblastic anemia.Disease of hematopoietic system infantile anemia（1）nutritional iron deficiency anemia(IDA)（2）nutritional megaloblastic anemia Primary/immunity thrombocytopenia Purpura(ITP)Leukemia haematogenesis of childrenhematopoiesis-produc

3、ed blood extramedullary before birth and postnatal mesoblast hepatic medullary 3-15w 6w-6ms 3ms Embryo stage Mesoblastic haematogenesis：3ws begin，8ws weaken,12-15ws disappears。liver：8ws begin，6months gradually weaken,erythroblast、granular cell and megakaryocyte.Embryo stage3、spleen：12ws begin erythr

4、ocyte,granule,lymphocyte4、Haematogenesis of lymphatic organ 1.thoracic gland:8ws 2.lymphatic nodes:11wsEmbryo stage5、myelo-haematopoiesis：6mons Haematogenesis function emphasis，make various kinds of blood cells，unique hematogenic organ after birth.Haematopoiesis postnatal 1、marrow：2、extramedullary：w

5、hen requirement of haemopoiesis increase，liver、spleen、lymphadenectasis，hepatomegaly and splenomegaly,in circulating blood immature erythrocytes and granulocytes.Physiological haemolysis Normal newborns have higher hemoglobin(HB)and hematocrit levels and a shortened survival period of the fetal RBCs

6、contributes to the development of physiologic anemia.Physiological haemolysis erythropoiesis abruptly ceases with onset of respiration at birth,when the arterial oxygen saturation rises toward 95%.levels of erythropoietin(EPO)are low.EPO has a decreased half-life and an increased volume of distribut

7、ion in newborns.A shortened survival of the fetal RBC also contributes to the development of physiologic anemia.the sizable expansion of blood volume that accompanies rapid weight gain during the first 3 mo of life adds to the need for increased RBC production.blood characteristics ages red blood ce

8、lls(RBC)and HbPhysiological haemolysis and anemia write blood cells(WBC)and classification 4-6 cross Platelets 150-250109/L blood volume 8-10%Red blood cell(RBC)Term newborns have a red cell mass that is higher than at any other time of life.an appropriate condition for the low oxygen environment of

9、 intrauterine life.The RBC count is 5.010127.01012,hemoglobin concentration is about 150220g/L at birth.The RBC and hemoglobin concentration in preterm infants are slightly lower than those in term infants.Red blood cell(RBC)The wide range of hemoglobin concentration is accounted for by:Variation in

10、 how rapidly the umbilical cord is clamped.An infants position after delivery.If cord clamping is delayed and the baby is held lower than placenta,both hemoglobin and blood volume are increased by a placental transfusion.Change of HB after birthReticulocyteReticulocyte Reticulocyte is 0.04-0.06 in t

11、he first 3 days.Reticulocyte decreases to 0.005-0.015 after 4-7 days.Reticulocyte rises to 0.02-0.08 in 4-6 weeks.Reticulocyte is equal to an adults after 5 months.White blood cell(WBC)The normal number of WBC is higher in infancy and early childhood than later in life.WBC count is 15109 20109 at bi

12、rth.After 612 hours,it rise to 21109 28109 and then begins to decrease to 12109 by 1 week.WBC count maintains about 10109 at infant period and approach adults WBC count level by 8 years.White blood cell(WBC)The change in WBC classification is the proportion between lymphocyte and granulocyte.Lymphoc

13、yte is about 30%and granulocyte is about 65%at birth,but the later lymphocyte contrary to neutrophile granulocyte decreases.The proportion between lymphocyte and granulocyte is equal at 46 days after birth.White blood cell(WBC)Lymphocyte is about 60%and granulocyte is about 35%subsequently.They are

14、equal at 46 years.After 7 years white cell classification in infants is similar to that in adult.4-6 DaysGranulocyteLymphocyte4-6 yearsChange of proportion in Lymphocyte and GranulocytePlatelet count Normal value for the platelet count are about 150250109/L and vary little with age.Blood volume Bloo

15、d volume in infants is more than in adults.The newborns blood volume is 10%of his weight and about 300ml on average.A childs is about 8%10%of his weight.AnemiaDefination:Anemia is defined as a reduction of the red blood cell volume or hemoglobin concentration below the range of values occurring in h

16、ealthy persons.Anemia is an absolute decrease in hematocrit,hemoglobin concentration,or the RBC count.Anemia is not a diagnosis,but a sign of underlying disease.The criteria of anemiaAgeHb concentration 28 days 145 g/L14 months 90 g/L46 months 100g/L6 months6 years 110g/L614 years 120g/L Anemia1.Cla

17、ssification 1）degree:mild moderate severe Very severe 2）Morphology of RBC3）Causes:lost blood,hemolytic,deficiency of forming Hb and RBC degree RBC(van/mm3)Hb(g/L)Mild 300-400 90-110 Moderate 200-300 60-90 Severe 100-200 30-60 Very severe 100 30 Morphologynanemia with microcytosis and hypochromianAne

18、mia with macrocytosisnAnemia with normalcytosis AnemiaMore anemia MCV MCH MCHCNormal 80-94 28-32 32-38Micro-hypochromia 80 28 94 32 32-38microcytosis 80 28 32-38 mean corpuscular volume(MCV),means corpuscular hemoglobin(MCH),mean corpuscular hemoglobin concentration(MCHC)Causes1.lost blood:acute chr

19、onic2.hemolysis Intrinsic membrane hereditary spherocytosis Glycolysis pyruvate kinase hemoglobin sickle cell,unstable Hb oxidation G6PD extrinsic:immune,infection,DICCauses 3.deficiency of forming Hb and RBC deficiency of hematopoiesis substance medullary hematopoiesis disorder(Aplastic anemia)The

20、inhibition of haematopoiesis induced by:Inflamation Chronic nephritis Toxicity Cancer cells invasion bone marrow Symptoms of anemia Asymptomatic:particularly if the anemia develops over a long time.General manifestation:pallor of the skin and mucous membranes,lethargy,malnutrition,growth retardation

21、.liver,spleen and lymph nodes expansion.Digestion system:anorexia,nausea and constipation.Symptoms of anemia Cardiovascular and respiratory system:tachycardias,increased artery pressure,wheeze and increased pulse.severe anemia may cause heart expansion and congestive cardiac failure.Nerver system:ve

22、rtigo,tinnitus,irritability,and disorders of attention.2.DiagnosisHistory positive manifestation laboratory tests Blood smear BM Hb ananysis Growth development nutrition nails fairs liver spleen and lymph notes 5 points:age,course,symptoms,feeding,past medical history,family history Morphology of RB

23、C,reticulocyte count,WBC,platelet count,bone marrow cell smear,HB,special examination3.Treatment Elimination etiology General Medicine Intravenous blood Transplantations:BM ,stem cells Other nutritional anemia with microcytosis and hypochromiaDefinition nutritional iron deficiency anemia(IDA)Hb、most

24、 common、6-24ms、special prevention Iron metabolism Iron content and distribution:2/3 of the iron is present in HB and 1/3 in tissue and transport form.Content of elemental iron(mg/kg)Adult females40Adult males50newborn75Iron metabolismIron absorption:The primary regulator of iron homeostasis is intes

25、tinal iron absorption.Iron absorption takes place primarily in the duodenum by the enterocytes at the tip of the intestinal villa.Iron must pass though the apical and the then the basolateral membranes of these cells to reach the circulation.Iron metabolismIron storage:Most body iron is contained in

26、 HB,with smaller amounts bound to ferritin(铁蛋白)and hemosiderin（含铁血黄素）in the reticuloendothelial system,myoglobin in muscle,circulating transferring,and iron-containing enzymes.The major iron stores are in the form of ferritin.As iron continues to accumulate in the cell,a second storage form,hemoside

27、rin appears.Iron metabolismIron characteristics:The fetus absorbs iron from the mother across the placenta.Term infants have adequate reserves for the first 4 months of life.Preterm infants have limited iron stores and because of their higher rate of growth,they outstrip their reserves by 8 weeks of

28、 age.Iron metabolismIron characteristics:At birth,because of“physiological haemolysis”,much iron is released to plasma and little iron is absorbed from food,During the second stage(about 2 months old),hematopoiesis is increased and more iron is absorbed from food,so iron deficiency is rare in this s

29、tage.After 4months,development increase,iron in food is deficient and iron stores exhaust,so most iron deficiency anemia occurs in 6 months to 2 years or 3 years old child.causes1.inadequate iron stores:preterm infant,twin2.intake iron deficiency3.growth and development increased iron requirement4.i

30、ron absorb abnormal5.a amount of iron loss:hookworm infestation,repeated venesection,Meckels diverticulum,recurrent epistaxis(反复鼻出血).pathogenesis IRON Hb microcytosis and hypochromia RBC Three stage of iron deficiencyDeficiency of iron progresses in stages iron depletion(ID):tissue iron stores are d

31、eleted,under normal condition,this correlates directly with decrease in the ferritin lever,reticulocyte percentage decreases.Iron deficient erythropoiesis(IDE):loss of circulating iron.Low serum iron less than 30ug/dl,low transferring saturation and/or elevated total iron binding capacity.Three stag

32、e of iron deficiency iron deficiency anemia(IDA):iron deficiency following depletion of both marrow store and circulating iron.IDIDEIDAclinical manifestation1.general manifestation:mild iron deficiency is Asymptomatic,pallor of the skin and mucous mebranes are most evident and lethargy,malnutrition,

33、growth retardation.2.liver spleen and lymph nodes enlarge3.digestion system:anorexia（食欲差）,nausea（恶心）,constipation（便秘）.diarrhea clinical manifestation 4.cardiovascular and respiratory manifestation:tachycardia,increased artery pressure,wheeze,increased pulse.Severe anemia may cause heart expansion an

34、d congestive cardiac failure.5.nervous system manifestation:vertigo,irritability.clinical manifestation Main signs may be pallor of the skin and mucous membranes.Severe anemia may cause congestive cardiac failure.IDA in infancy and early childhood is associated with developmental delay and poor grow

35、th.laboratory test1.blood smear2.bone marrow3.iron metabolism Inequality of size of erythrocytes，small cell，Central olistherozone obviously hypercellular,erythroid hyperplasia,the development of cytoplasm falls behind nucleus.leukocytes and megakaryocytes are normal.Bone marrow iron stain：ferruginat

36、ion grains in the erythocytes.Normal bone marrow iron stain正常骨髓铁染色正常骨髓铁染色IDA iron stain铁缺乏骨髓铁染色铁缺乏骨髓铁染色laboratory test The decrease of HB concentration is more than the decrease of red cells count.Blood smear reveals the more feature of microcyte and hypochromia.MCV80fl,MCH26pg,MCHC0.31.Reticulocyte

37、 is normal or slightly decreases.WBC and platelets are normal.Blood count in iron deficiencyHB75g/L120g/LRBC3.541012/L4.241012/LMCV64fl86flMCHC18.5pg32pgreticulocyte1.3%1.4%WBC7.54109/L7.64109/Lproportionnormalnormalplatelet254109/L257109/Llaboratory test Bone marrow reveals increased basophilic nor

38、moblast and polychromatic normoblast.Granulocyte system and megakaryocyte system are normal.Iron metabolisms Serum ferritin(SF)(血清铁蛋白)Free erythrocyte protoporphyrin(FEP)Serum iron,total iron binding capacity Iron in bone marrow Iron metabolismsIron study ID IDEIDASerum ferritin(SF)Iron store Red bl

39、ood cell protoporphyrin(FEP)N Percent sideroblasts N Serum iron NN/diagnosis first consider-history+clinical manifestation+blood smear Decide diagnosis-bone marrow+iron metabolism May be see treatment with iron (The bone marrow is hypercellular,with erythroid hyperplasia,the normoblasts may have sca

40、nty,and the development of cytoplasm falls behind one of nucleus.leukocytes and megakaryocytes are normal.)treatment 1.nursing feeding 2.get rid of etiology 3.iron medicine 4.interfusions bloodOral administration of simple ferrous salts ferrous sulfate(硫酸亚铁)ferrous gluconate（葡萄糖酸亚铁）ferrous fumaratep

41、olysaccharide iron Dosage:4-6mg/kg elemental iron per day Oral iron preparation Administration the iron prior to meals/between to meals.Administration ascorbic acid with iron preparation.Therapeutic course:withdrawal of iron preparation 6-8 weeks after hemoglobin recover to normal level or when SF(S

42、erum ferritin)and FEP(Free erythrocyte protoporphyrin)is normal.Oral iron preparationParenteral iron preparation To be administered only for gastrointestinal malabsorption or severe intolerance prevents effective oral iron therapy.Parenteral iron preparation A parenteral iron preparation(iron dextra

43、n)is an effective form of iron and is usually safe when given in a properly calculated dose,but the response to parenteral iron is no more rapid or complete than that obtained with proper oral administration of iron,unless malabsorption is a factor.Blood Transfusion With a severe anemia,immediate re

44、d blood cell transfusion may advisable,especially in cardiac failure or severe infection,but volume and speed of transfusion must be controlled well.We may transfuse,severely anemia children should be given only 2-3ml/kg of packed cells at any one time.If there is evidence of frank congestive failur

45、e,a modified exchange transfusion using fresh-packed RBCs should be considered.Iron therapyNotice:3 points1.Injection iron in danger 2.Reaction:12-24h(irritability,appetite)-36-48h(erythroid hyperplasia)-48-72h(reticulocytosis)-5-7ds(peaking)2-3ws to reticulocytes3.Times:6-8wsPrevention4 points moth

46、er milk feeding specter food with iron preterm infant Nutritional megaloblastic anemia Folic acid and vitamin B12 deficiency are primary causes of megaloblastic anemia.The clinical features include anemia，the decrease of red cell is more than that of HB，the volume of red cell is larger than normal.C

47、auses 1.less intake 2.absorb abnormal 3.drug interactions 4.requirement increased Pathogenesis folic acid folic acid with 4 hydrate vitamin B12 DNA Hb very large RBC Megaloblastic with Lot of Hb dihydrofolate reductase(THFA)VitaminB12 is importance in synthesis of nerve.deficiency of vitaminB12 can

48、lead to discord of neurology psychology.In the macrocytic anemia produced by deficiency of vitamin B12,the symptoms and signs include those of anemia and neuropathy.nVitamin B12 deficiency neurology psychology symptom Patients develop a demyelinating lesion of neurons of the spinal column and cerebr

49、al cortex.This condition results in paresthesias of the hands and feet,unsteadiness of gait,and eventually memory loss and personality changes.There is retard of intellective and physical development.Trembling of Extremities or head,hypertension of muscle,tendon reflex reinforcement,positive Babinsk

50、is sign may appear.Clinical manifestation1.General features:puffiness,poor nutrition,hair yellowed,mild edema,petechia(plt),mucocutaneous hemorrhage.2.feature of anemia:lethargy,extramedullary3.neurology psychology:irritability,vertigo.4.digestive symptoms:anorexia,nausea,diarrhea.Laboratory tests 1

51、.blood smear 2.bone marrow3.blood biochemistry tests4.othersvariation in BRC shape and size,macrocytosis,reticulocyte count is low,nucleated RBCs and megaloblastic morphology are often seen,thrombocytopenia Hypercellular,Megaloblastic changes,hypersegmentation Laboratory tests Blood routine examinat

52、ion:macrocytic anemia,the decrease of red cell count is more than the decrease of HB.MCV94fl,MCH32pg.Rreticulocyte is decrease.WBC and platelets are also decreased.Bone marrow:increased basophilic normoblast and polychromatic normoblastic.Granulocytic system and megakaryocyte system:normal/less than

53、 normal.Laboratory tests Vitamine B12:normal serum vitamin B12 levels range from 200-800ng/L,B1212ng/L reveals B12 deficiency.Folate:normal serum folate levels range from 5-6ug/L,folate 3ug/L reveals deficiency.others:LDH:serum lactic dehydrogenase(LDH)is increaseDiagnosis first consider-history+cli

54、nical manifestationMarked symptoms and signs of central nervous system.(it supports defiency of vitamin B12.)+.blood smear decide diagnosis-.bone marrow+metabolism(To distinguish the deficiency of folic acid with the deficiency of vitamin B12.)maybe see treatment with medicine Treatment1.nursing fee

55、ding 2.get rid of etiology 3.medicine vit B12,folic acid Vitamin B12 preparation Vit B12 preparation to treat vit B12 deficiency.Not to use folic acid preparation in patients with vitB12 deficiency only.Intramuscular administration of vit B12 0.5-1 mg，QW or 100g，BiW，usually with reticulocytosis in 2

56、-4 days,unless there is concurrent inflammatory disease.If there is evidence of neurologic involvement,1 mg should be injected intramuscularly daily for at least 2 wk.Maintenance therapy is necessary throughout a patients life；monthly intramuscular administration of 1 mg of vit B12 is sufficient.Fol

57、ic acid preparation .Folic acid may be administered orally in a dose of 15 mg/24 hr.If the specific diagnosis is in doubt,125 mg/24 hr of folate may be used for a week as a diagnostic test.vitamine C will help absorption of folate.IDAmegaloblastic anemiaage6m-2y6m-2yCauseiron VtB12/folic acidClinica

58、l manifestationpallorpuffinessextramedullary Nervous systemslightstrikingIDAmegaloblastic anemiaBlood smearmicro-hypochromiamacrocytosisBone marrowcytoplasm falls behind nucleusMegaloblastic changesIron metabolismabnormalNVtB12/folic acidN In this case,macrocytic anemia is caused by deficiency of vi

59、tamin B12.Why?In the macroblastic anemia produced by deficiency of vitamin B12,the symptoms and signs include those of anemia and neuropathy.Patients develop a demyelinating lesion of neurons of the spinal column and cerebral cortex.This condition results in paresthesias(感觉异常)of the hands and feet,unsteadiness of gait,and eventually memory loss and personality（智力）changes.There is retard of intellective and physical development.Trembling（震颤）of Extremities or head,hypertension of muscle,tendon reflex reinforcement,positive Babinskis sign may appear.Final diagnosisDiagnosis TreatmentTherapy