《儿科学》课程教学资源（授课教案）10 Nutritional Iron Deficiency Anemia

重庆医科大学儿科学教案造血系统疾病一营养性贫血教师：于洁授课题目TEACHING TOPIC Nutritional Anemia第几次课TIMES7th教学方法METHODSClass teaching教学对象OBJECTIVESevenstudents2005,yearsGrade200720062004.2003.2002.2001学时：TIME80 minutes授课目的PURPOSEStudythe IDA.Knows how to diagnosis and treat the anemia,aswell as the preventionLearn the diagnosis and treatment of the MA本课重点EMPHASISEtiology forIDAand preventionDiagnosis and treatment of the IDA本课难点 DIFFICULTIESIron metabolism of the IDA深化与拓宽Emphasis the social importance; compare our data with othersThe developmentstoshowthesocial-economicimpactonthedisease2Emphasis the iron deficiency to neurology3)Differential mainly for infectious anemia and thal;4) Emphasis on the prevention英语要求All inEnglishIDA: ron deficiency anemia;English requirementsIDE:iron deficiency erythropoiesisID: iron deficiency;MA: megaloblastic anemia践性教学安排Clinically, combined with the patients to learn the manifestationsClinical studyand Lab features; To find out the cause of IDA by history taking;discuss the diagnossi and differential. Order the medication for thepatients.Andtheeducation planfor教材TEXTBOOKUSEDYang Xiqiang Chief Editor,《PEDIATRICS》 6th Edion, People'sHealth Publication,2003及参考资料REFERENCES1.胡亚美,江载芳．诸福棠实用儿科学.第7版.北京：人民卫生出版社,20022. Behrman RE, Kliegman RM and Jenson HB. Nelson textbook opediatrics.16th ed. Science Press, Harcourt Asia, W.B.Saunders, 2001

重庆医科大学儿科学教案 造血系统疾病－营养性贫血 教师：于洁 授课题目TEACHING TOPIC Nutritional Anemia 第几次课 TIMES 7 th 教学方法 METHODS Class teaching 教学对象 OBJECTIVE Seven years students in Grade 2007, 2006 ， 2005, 2004,2003,2002,2001 学时: TIME 80 minutes 授课目的 PURPOSE Study the IDA. Knows how to diagnosis and treat the anemia, as well as the prevention Learn the diagnosis and treatment of the MA 本课重点 EMPHASIS Etiology for IDA and prevention Diagnosis and treatment of the IDA 本课难点 DIFFICULTIES Iron metabolism of the IDA 深化与拓宽 The developments 1) Emphasis the social importance; compare our data with others to show the social-economic impact on the disease 2) Emphasis the iron deficiency to neurology 3) Differential mainly for infectious anemia and thal； 4) Emphasis on the prevention 英语要求 English requirements All in English IDA: Iron deficiency anemia； IDE: iron deficiency erythropoiesis ID: iron deficiency; MA: megaloblastic anemia 践性教学安排 Clinical study Clinically, combined with the patients to learn the manifestations and Lab features; To find out the cause of IDA by history taking; discuss the diagnossi and differential. Order the medication for the patients. And the education plan for 。 教材 TEXT BOOK USED Yang Xiqiang Chief Editor，《PEDIATRICS》6th Edition，People’s Health Publication，2003 及参考资料 REFERENCES 1. 胡亚美,江载芳. 诸福棠实用儿科学.第 7 版.北京:人民卫生出版 社,2002 2. Behrman RE, Kliegman RM and Jenson HB. Nelson textbook of pediatrics.16th ed. Science Press, Harcourt Asia, W.B. Saunders, 2001

3. Nathan and oski Hematology of infancy and childhood (7ih2009)教具TEACHINGAIDSPPT教具PPT教学程序Procedures详细见讲稿主要内容及安排（教学内容详细安排、教学方法的运用、师生活动设计、及时间分Details seethecontents and配)arrangement The contents and Arrangements讲稿主要内容及安排meanstimeminNutritional Iron Deficiency Anemia (N-IDA)PPT80INTRODUCTION)51.N-IDA Definition /describingReviewtheThe anemia caused by insufficient dietary iron uptake,in which the iron storage andaneminhemoglobin synthesis decreaseddefinition2.Clinical characteristicsandclassication.+iron stores+serum iron.hmintanhmmoyicaQuestion:good response toirontherapy6mo to 3 yrsthemost3. IncidencecommonIn China,1980s data showed that the incidence ofIDAin some city was about 35-40%anemiainInthe United Saesabout 9%f2yldsareiron deficien3%haveanmachildreadolescent girls, 9% are iron deficient and 2% have anemia. In boys, a 50% decrease instored iron occurs as puberty progress15[ron metabolism] :Using table1.Iron contents and compartment :topresentCONTENTS:the detailedNew born 75mg/kg: Children35-70mg/kg,Adults M 50mg/kg,F 35mg/kgThedata.3CMOPARTMENT:compartmeHemoglobin 64%, Storage iron 30%--ferritin/Hemosiderinnt indicatethe functionMyloglobin 3%;Enzyme iron 0.4%; Serum iron 0.4

3. Nathan and oski Hematology of infancy and childhood (7th2009) 教具 TEACHING AIDS PPT 教具 PPT 教学程序 Procedures （教学内容详细安排、教学方法的运用、师生活动设计、及时间分 配） 详细见讲稿主要内容及安排 Details see the contents and arrangement The contents and Arrangements 讲稿主要内容及安排 means time min Nutritional Iron Deficiency Anemia (N-IDA) PPT 80 [INTRODUCTION] 5 1.N-IDA Definition / describing The anemia caused by insufficient dietary iron uptake, in which the iron storage and hemoglobin synthesis decreased. Review the anemin definition and classication. Question: the most common anemia in children. 2.Clinical characteristics ⚫  iron stores  serum iron ⚫ hemoglobin concentration , hypochromic microcytic anemia, ⚫ good response to iron therapy. ⚫ 6mo to 3 yrs. 3. Incidence In China, 1980s data showed that the incidence of IDA in some city was about 35-40%. In the United Sates, about 9% of 1-2 yr-olds are iron deficient; 3% have anemia. Of adolescent girls, 9% are iron deficient and 2% have anemia. In boys, a 50% decrease in stored iron occurs as puberty progress. [Iron metabolism]： 15 1.Iron contents and compartment： CONTENTS: New born 75mg/kg; Children35-70mg/kg;Adults M 50mg/kg, F 35mg/kg. CMOPARTMENT: Hemoglobin 64%; Storage iron 30%-ferritin/Hemosiderin; Myloglobin 3%; Enzyme iron 0.4% ; Serum iron 0.4 Using table to present the detailed data. The compartme nt indicate the function 3

2.Iron sourRelated toHemoglobin ironthe deficienttuallyinaoseowhich itcycles almost endlesslyfrom the plasma to the developing erythroblast (whereitreasonis utilized in hemoglobin synthesis), thence into the circulating blood for about 4 monthsHelptoand then to phagocytic macrophages. Here it is removed from hemoglobin and releasednderstandackintepeat in the cyclthe etilogyDietary ironHigh in iron: Red meat/ liver kidney/ oily fishAverage iron: Beans / fortified cereals/ dark geen vegetablesl dried fuit/ nuts andeedsPoor in iron: milkIron absorption1-20%general absorption10-25%Meat/ fish/ chicken1% Cereals/vegetables50%/10%Breast/cow's milk3.Iron absorpEmphasison and transportatiorIron is absorbed at brush border of epithelia cells of the intestinal villi, particularly inonthethe duodenum (djue'dinem) and upper jejunum. It is absorbed in the form of heme or asprocesferric or ferrous irons.In human little of theheme absorbed by mucosal cells passe:understandidirectlyfromknd ferric has to be changed into ferrintKnowingcombinethe plasma. Iron may also be trapped in the ferrtiwithintheepithelial cells of the gastrointestinal tract, thereby preventing its absorption when bodythe conceptsiron stores are high With the passage of time the mucosal cells advances to the tip of the aboutSI/TIBC/TSvillis, is sloughed and lost in the feces together with it's retained iron.Learn abouthectionoftlerrin is to move iron fronsport protein transfeSOwherever it enters the plasma to the erythroblasts of the marrow. It binds toregulation.TfR on the erythroblast membrane. Relatively small amounts of iron areIntroducetransported to other tissues, especially in a slow exchange with the iron inwith figureferitin and hemosiderin and to a much lesser extent with other tissue forms ofto show theirorprocessoximately one third of the transferrin iron binding sites areorly.approoccupied by iron. This complex is clled serum iron (SI)Theserumconcentration of transferrin is called total iron banding capacity (TIBC). Thestate of transferin combined with iron is described by transferin saturation(TS).4.Requirement and excretionIndicate that 1demandthe infantsexcretion

2.Iron sources Hemoglobin iron Once an atom of iron enters the body, it is virtually in a closed system in which it cycles almost endlessly from the plasma to the developing erythroblast (where it is utilized in hemoglobin synthesis), thence into the circulating blood for about 4 months, and then to phagocytic macrophages. Here it is removed from hemoglobin and released back into the plasma to repeat in the cycle. Related to the deficient reason. Help to nderstand the etilogy 4 Dietary iron High in iron: Red meat/ liver kidney/ oily fish Average iron: Beans / fortified cereals/ dark green vegetables/ dried fruit/ nuts and seeds Poor in iron : milk Iron absorption: general absorption 1-20% Meat/ fish/ chicken 10-25% Cereals/vegetables 1% Breast/cow’s milk 50%/10% 3.Iron absorption and transportation Iron is absorbed at brush border of epithelia cells of the intestinal villi, particularly in the duodenum (djue’di:nem) and upper jejunum. It is absorbed in the form of heme or as ferric or ferrous irons. In human little of the heme absorbed by mucosal cells passes directly into plasma. Ferrous from heme and ferric has to be changed into ferric to combine with transferrin in the plasma. Iron may also be trapped in the ferrtin within the epithelial cells of the gastrointestinal tract, thereby preventing its absorption when body iron stores are high. With the passage of time the mucosal cells advances to the tip of the villis, is sloughed and lost in the feces together with it’s retained iron. The major function of the transport protein transferrin is to move iron from wherever it enters the plasma to the erythroblasts of the marrow. It binds to TfR on the erythroblast membrane. Relatively small amounts of iron are transported to other tissues, especially in a slow exchange with the iron in ferritin and hemosiderin and to a much lesser extent with other tissue forms of iron. Normally, approximately one third of the transferrin iron binding sites are occupied by iron. This complex is called serum iron (SI). The serum concentration of transferrin is called total iron banding capacity (TIBC). The state of transferrin combined with iron is described by transferrin saturation (TS). Emphasis on the process understandi ng. Knowing the concepts about SI/TIBC/TS Learn about some regulation. Introduce with figure to show the process. 8 4.Requirement and excretion demand excretion Indicate that the infants 1

1mg/d1mg/drequiredults 4mo-3yr1mg/kg(15ug/kg/d)morethanpremature2mg/kgexcretion.[ETIOLOGY]8Pooriron storeVeryPoor dietary intake of ironimportant toOverdevelopknow,Chronic bleedingEmphasisNeed tocombinewiththeironmetabolismfeatures infetus and youngchildrenon the poorintake for【Pathogenesis]Reviewtheirond+protoporphyri-heme(+globins)=hemoglobinprocessofHbformingHypochromic /microcytic RBC formingThree stages:ID (Iron deficiency)-IDE (Iron deficiency erythropoiesis) --IDAEnzymes,Immunefunction;Skin/mucosalvIP【临床表现】5RecognizinGeneralFaturesgTheonsetofthAhdegeefanmag the pallor,Pallor; Extramedullary hematopoiesispayMild/Severe conditionattention toDigestivesystemCardiacfunctionImmunefunctionthe effectsNeurology/ intellectual: Preliminary reports suggest that iron deficiency affectsofotherattention span, alertness, and learning of both young children and adolescents,systemseven when the degree of anemia is not severe. These have been linked toalteration of iron-containing enzymes and cytochromes[Lab studying ]VIPSIDA stages

adults 1mg/d 1mg/d 4mo-3yr 1mg//kg (15ug/kg/d) premature 2mg/kg require more than excretion. 【ETIOLOGY】 8 • Poor iron stores • Poor dietary intake of iron* • Overdevelop • Chronic bleeding Need to combine with the iron metabolism features in fetus and young children . Very important to know; Emphasis on the poor intake for 【Pathogenesis】 7 iron+protoporphyri－heme(+globins)= hemoglobin Review the process of Hb forming Hypochromic / microcytic RBC forming Three stages: ID ( Iron deficiency) –IDE ( Iron deficiency erythropoiesis) -IDA. Enzymes; Immune function ; Skin/mucosal 【临床表现】 VIP 5 General Features : Age; The onset of the IDA; The degree of anemia Recognizin g the pallor, pay attention to the effects of other systems Pallor; Extramedullary hematopoiesis; Mild/ Severe condition Digestive system; Cardiac function ; Immune function Neurology/ intellectual: Preliminary reports suggest that iron deficiency affects attention span, alertness, and learning of both young children and adolescents, even when the degree of anemia is not severe. These have been linked to alteration of iron-containing enzymes and cytochromes. [Lab studying ] VIP 8 IDA stages

Learn aboutPeripheral bloo:Microcytic/Hypochromimicrocytic Hemoglobin level/hypochromRBC:↓MCV <80fl,↓MCH <26ug,↓MCHC<0.31ic anemia,Bone marrowanKnows ironIron related metabolismrelateddetection+sI:<9-10.7umo/L(12.8-31.3umol/L)Knows thedifferencesor<50-60ug/dl (75-175ug/dl)thedifferent↑ TIBC : >62.7umol/L(>350ug/dl)stages+TS:<15% （30-50%)IDE: SFI,FEPt (>0.9umo/Lor>50ug/dl)ID : SF<12ug/L/marrow iron3+5[Diagnosis & DIFFERENTIAL]Diagnosis:by the following considerationsImportantImpression : age, feeding, PBIDiagnosis : biochemical changeProven by therapyDifferential diagnosisLearntheChronic & inflammatory diseasesname of theThalassemiadiseasesPulmonary hemosiderosis.Siderblasticanemia10Treatment and PreventionTreatments:General care:rest for hear,nutrition, avoid infectionEradicatethe causes*: as the above reasons forIDAIron therapy*Elemental iron:4-6mg/kg/d,Oral medication,Ferrous firstAdministration Between meals; Vitamin C; CourseTransfusion:in case ofthe severe anemiaObserve the responsesresponse12-24hrReplacement of iron enzymes,subjective improvement36-48hrInitial marrowresponse:erythroidhyperplasi

Peripheral blood：Microcytic/Hypochromic  Hemoglobin level RBC:  MCV < 80fl,  MCH < 26ug,  MCHC < 0.31 Bone marrow: Erythroid hyperplasia, Stainable iron Iron related metabolism  SI： < 9-10.7umol/L (12.8-31.3umol/L) or < 50-60ug/dl (75-175ug/dl ）  TIBC： > 62.7umol/L (>350ug/dl)  TS： < 15% （30-50%） Learn about microcytic /hypochrom ic anemia; Knows iron related detection. Knows the differences at the different stages IDE: SF↓,FEP↑（>0.9umol/L or> 50ug/dl) ID： SF < 12ug/L / marrow iron 【Diagnosis & DIFFERENTIAL】 3+5 Diagnosis: by the following considerations • Impression：age, feeding, PBL • Diagnosis：biochemical change • Proven by therapy Important Differential diagnosis • Chronic & inflammatory diseases • Thalassemia • Pulmonary hemosiderosis • Siderblastic anemia Learn the name of the diseases [Treatment and Prevention] 10 Treatments: • General care: rest for hear; nutrition; avoid infection. • Eradicate the causes*: as the above reasons for IDA. • Iron therapy*: Elemental iron： 4-6mg/kg/d; Oral medication; Ferrous first ; Administration Between meals; Vitamin C; Course • Transfusion: in case of the severe anemia Observe the responses: time response 12-24 hr Replacement of iron enzymes,subjective improvement 36-48 hr Initial marrow response: erythroid hyperplasia