nutritional anemias in children.ppt

NUTRITIONAL ANEMIAS IN CHILDRENNUTRITIONAL ANEMIAS IN CHILDREN

DR.M.DASARADHA RAMI REDDYDR.M.DASARADHA RAMI REDDY M.D.,D.C.H.,M.D.,D.C.H.,

PROF OF PEDIATRICS,PROF OF PEDIATRICS,KIMS,NARKETPALLYKIMS,NARKETPALLY

Overview Overview

DefinitionDefinitionNutrients in hematopoesisNutrients in hematopoesisPrevalence Prevalence Common nutritional anemiasCommon nutritional anemias Iron deficiency anaemia (IDA)Iron deficiency anaemia (IDA)Megaloblastic anemias Megaloblastic anemias

ANEMIAANEMIA

What is Nutritional Anemia:What is Nutritional Anemia:

Reduced Red blood cell mass due to Reduced Red blood cell mass due to deficiency of nutrients required for deficiency of nutrients required for RBC’s.RBC’s.

Nutrients required for RBC Nutrients required for RBC productionproduction

Proteins Proteins FatsFatsVitamins Vitamins Trace elements etc Trace elements etc

55

Nutrients required for RBC Nutrients required for RBC production production

Proteins- all essential amino acids are Proteins- all essential amino acids are necessary; methionine deficiency – necessary; methionine deficiency – megaloblastic anemiamegaloblastic anemia

Vitamins-Vitamins- - - BB1212 and folic acid and folic acid – megaloblastic anemia – megaloblastic anemia --CC- Fe- Fe++++++ to Fe to Fe++++ & Releases Fe from stores. & Releases Fe from stores. --AA- mobilises Fe from stores & improves - mobilises Fe from stores & improves

utilisation utilisation --B6B6- macro/micro anemia,- macro/micro anemia, --B2B2- BONE MARROW-hypoplasia---- - BONE MARROW-hypoplasia---- Trace elements: iron,copper zinc Trace elements: iron,copper zinc In PEM and other hematopoietic nutrient(s) In PEM and other hematopoietic nutrient(s)

anemia on ‘Fe- suppl’ –alone – will have poor anemia on ‘Fe- suppl’ –alone – will have poor response.response.

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Prevalence of nutritional anemia Prevalence of nutritional anemia

ICMRICMR – –1999-2000- 11 states 19 districts 1999-2000- 11 states 19 districts 84.6% (Hb <7.0 g/dl-84.6% (Hb <7.0 g/dl- 9.9% ).9.9% ).

90%90% adolescentsadolescents were also anemic Teoteja were also anemic Teoteja

et al 2000.et al 2000.

>80% <>80% < 3 yr children3 yr children are anemic NFHS-II& are anemic NFHS-II& Agarwal et al.Agarwal et al.


COMMON NUTRITIONAL ANEMIASCOMMON NUTRITIONAL ANEMIAS

DEFICIENCY OFDEFICIENCY OF

IRONIRON

FOLIC ACIDFOLIC ACID

VITAMIN B12VITAMIN B12

IRON DEFICIENCY ANEMIA ( I D A )IRON DEFICIENCY ANEMIA ( I D A )

““Iron is not like gold that glitters or silverIron is not like gold that glitters or silver

that shines, however,it outshines both inthat shines, however,it outshines both in

its biological importance”its biological importance”All adolescents across the country shouldAll adolescents across the country should

have at least 12 gm% Hb by 12 years of have at least 12 gm% Hb by 12 years of

age age (12 by 12 initiative programme)(12 by 12 initiative programme)


IRON DEFICIENCY ANEMIA ( I D A )IRON DEFICIENCY ANEMIA ( I D A )

MOST COMMON HEMATOLOGICAL DISEASE IN MOST COMMON HEMATOLOGICAL DISEASE IN INFANCYINFANCY

MOST COMMON NUTRITIONAL ANEMIA IN MOST COMMON NUTRITIONAL ANEMIA IN INFANCYINFANCY

30% OF GLOBAL POPULATION SUFFERS FROM IT30% OF GLOBAL POPULATION SUFFERS FROM IT

IN INDIA IT IS 50%IN INDIA IT IS 50%

IT AFFECTS CHILD DEVELOPMENT&BEHAVIOURIT AFFECTS CHILD DEVELOPMENT&BEHAVIOUR

Destribution of ironDestribution of iron

Iron containing enzymesIron containing enzymes

NUTRITIONAL ANEMIAS IN CHILDREN-IDANUTRITIONAL ANEMIAS IN CHILDREN-IDA

SOURCES OF IRONSOURCES OF IRON

ANIMAL-MEAT,LIVER,KIDNEY,EGG YOLKANIMAL-MEAT,LIVER,KIDNEY,EGG YOLK

VEG-PULSES,BEANS,GREEN VEGETABLESVEG-PULSES,BEANS,GREEN VEGETABLES

PEAS,FRUITS.PEAS,FRUITS.

HUMAN MILK-0.29-0.45mg/dlHUMAN MILK-0.29-0.45mg/dl

COW’S MILK- 0.01-0.38mg/dlCOW’S MILK- 0.01-0.38mg/dl


IRON CONTENT OF NEW BORN-0.5gIRON CONTENT OF NEW BORN-0.5g

IRON CONTENT OF ADULT - 5gIRON CONTENT OF ADULT - 5g

ABSORPTION OF DIETARY IRON-10%ABSORPTION OF DIETARY IRON-10%

DAILY REQUIREMENT 8-10mgDAILY REQUIREMENT 8-10mg

+ve BALANCE REQUIRES 1mg/day+ve BALANCE REQUIRES 1mg/day

IRON IS ABSORBED MORE FROM BREASTIRON IS ABSORBED MORE FROM BREAST

MILK.MILK.


DIETARY IRON IS IN FERRIC FORMDIETARY IRON IS IN FERRIC FORMABSORBED IN FERROUS FORMABSORBED IN FERROUS FORMGASTRIC SECRETIONS DISSOLVE IRON &FORM SOLUBLE GASTRIC SECRETIONS DISSOLVE IRON &FORM SOLUBLE COMPLEXES WITH ASCORBIC ACIDCOMPLEXES WITH ASCORBIC ACIDSOLUBLE COMPLEXES REDUCED TO FERROUS FORM BY SOLUBLE COMPLEXES REDUCED TO FERROUS FORM BY FERRIC REDUCTASE &ABSORBEDFERRIC REDUCTASE &ABSORBEDIRON BINDS TO TRANSFERRIN IN PLASMAIRON BINDS TO TRANSFERRIN IN PLASMATRANSFERRIN-IRON TRANSPORT PROTEIN TRANSFERRIN-IRON TRANSPORT PROTEIN FERRITIN-STORAGE FORM OF IRONFERRITIN-STORAGE FORM OF IRONIRON IS STORED IN R E SYSTEM AS FERRITIN.IRON IS STORED IN R E SYSTEM AS FERRITIN.IRON ALSO STORED IN B M AS HEMOSIDERINIRON ALSO STORED IN B M AS HEMOSIDERINTRANSFERRIN RECEPTORTRANSFERRIN RECEPTOR

Nutritional anemias in children-IDANutritional anemias in children-IDA

Blood stream

Mucosal Cell

Hem Iron GI Lumen Non hem Iron

Dietary Iron

TRANSFERRIN To tissues

Carrier

To stores (ferritin)

Fe

METABOLISM OF IRON

Nutritional anemias in children-IDANutritional anemias in children-IDA

Daily iron cycleDaily iron cycle


REGULATION OF IRON ABSORPTIONREGULATION OF IRON ABSORPTION

DIETARY FACTORSDIETARY FACTORS

Physico –chemical form (ferrous formPhysico –chemical form (ferrous form better absorbed), better absorbed),

Other dietary constituents (phosphates, phytates,Other dietary constituents (phosphates, phytates,

calcium, tannic acid, etc.), calcium, tannic acid, etc.),

Iron doseIron dose

HOST FACTORS-Iron storesHOST FACTORS-Iron stores

OTHER FACTORSOTHER FACTORS

Rate of erythropoiesis,Rate of erythropoiesis,

Physiological statePhysiological state

Gastric juiceGastric juice

STAGES OF IRON DEPLETIONSTAGES OF IRON DEPLETION

Overload Normal Depleted ID IDA Stores

Serum ↑↑ N ↓↓ ↓↓ ↓↓↓↓Ferritin

Transferin ↑↑ N N ↓↓ ↓↓Satur.

Erythrocyte N N N ↑↑ ↑↑↑↑Protoporph.

MCV N N N N ↓↓

Hemoglobin N N N N ↓↓


CAUSES OF IRON DEFICIENCY ANEMIACAUSES OF IRON DEFICIENCY ANEMIA

DIMINISHED INTAKEDIMINISHED INTAKE

DIMINISHED ABSORPTIONDIMINISHED ABSORPTION

DEFECTIVE METABOLISMDEFECTIVE METABOLISM

CHRONIC BLOOD LOSSCHRONIC BLOOD LOSS

DIMINISHED STORESDIMINISHED STORES

INCREASED DEMANDSINCREASED DEMANDS


DIMINISHED INTAKEDIMINISHED INTAKE Not breast feeding,Cow’s milk feedingNot breast feeding,Cow’s milk feeding Iron poor dietIron poor diet

DIMINISHED ABSORPTIONDIMINISHED ABSORPTION MalabsorptionMalabsorption High level of inhibitorsHigh level of inhibitors

DEFECT IN METABOLISMDEFECT IN METABOLISM Idiopathic pulm. HemosiderosisIdiopathic pulm. Hemosiderosis Sideroblastic anemiaSideroblastic anemia Congenital transferrin deficiencyCongenital transferrin deficiency


CHRONIC BLOOD LOSSCHRONIC BLOOD LOSS Occult bleeding (erosive gastritis, drug Occult bleeding (erosive gastritis, drug

induced Recurrent diarrhea)induced Recurrent diarrhea) HookwormHookworm PolyposisPolyposis Prolapse rectumProlapse rectum Portal hypertensionPortal hypertension DysenteryDysentery Meckel’s diverticulumMeckel’s diverticulum Hiatus herniaHiatus hernia CephalhematomaCephalhematoma


DIMINISHED STORESDIMINISHED STORES Preterm & small for date babies,TwinsPreterm & small for date babies,Twins Early cord clamping (100ml of blood),APHEarly cord clamping (100ml of blood),APH Feto-fetal or feto-maternal transfusionFeto-fetal or feto-maternal transfusion

INCREASED DEMANDINCREASED DEMAND Rapid catch up growth in preterm and Rapid catch up growth in preterm and

SFDSFD Infancy & pubertyInfancy & puberty


CLINICAL FEATURESCLINICAL FEATURES

Pallor, pica, dull, irritable, poor appetitePallor, pica, dull, irritable, poor appetite Failure to thrive, easily fatiguedFailure to thrive, easily fatigued Frequent infectionsFrequent infections Decreased attention span, poor school Decreased attention span, poor school

performance, cognitive impairmentperformance, cognitive impairment Malabsorption and protien loosing Malabsorption and protien loosing

enteropathyenteropathy


CLINICALFEATURESCLINICALFEATURES

Tongue papillae are atrophiedTongue papillae are atrophiedNails-flat, thin, brittle, spoon Nails-flat, thin, brittle, spoon

shaped (koilonychia)shaped (koilonychia)Splenomegaly in 15%Splenomegaly in 15%Severe – cardiomegaly & CCFSevere – cardiomegaly & CCF


LAB DIAGNOSIS OF I D ALAB DIAGNOSIS OF I D A PBSPBS Low HemoglobinLow Hemoglobin Low HematocritLow Hematocrit Low Mean Corpuscular VolumeLow Mean Corpuscular Volume Serum ironSerum iron Serum Ferritin <10ng/mlSerum Ferritin <10ng/ml Transferrin Saturation<15%Transferrin Saturation<15% TIBC>350TIBC>350µµg/dlg/dl Increased free erythrocyteprotoporphyrinIncreased free erythrocyteprotoporphyrin


LAB DIAGNOSIS OF I D ALAB DIAGNOSIS OF I D A Bonemarrow staining Bonemarrow staining Reticulocyte hemoglobin contentReticulocyte hemoglobin content Stool examinationStool examination Lead estimationLead estimation


DIFFERENTIAL DIAGNOSISDIFFERENTIAL DIAGNOSISß-THALASSEMIA TRAIT-INCREASED HB A2 & FETALHB,ß-THALASSEMIA TRAIT-INCREASED HB A2 & FETALHB,

S.IRON,TIBC-NORMALS.IRON,TIBC-NORMAL RBC COUNT IS ELEVATEDRBC COUNT IS ELEVATED

RDW IS NORMAL(IDA-RDW IS NORMAL(IDA-RDW^)RDW^)

LEAD POISONING- LEAD POISONING- ELEVATED BLOODLEAD,FEP &ELEVATED BLOODLEAD,FEP &

URINARY COPROPORPHYRIN LEVELSURINARY COPROPORPHYRIN LEVELS


THERAPY OF I D ATHERAPY OF I D A Treat underlying causeTreat underlying cause Oral iron therapyOral iron therapy Dietary measuresDietary measures Activity restrictionActivity restriction Surgery Surgery


THERAPY OF I D ATHERAPY OF I D A

Oral iron therapyOral iron therapy 3-6mg/kg in 3 divided doses ( Hb rises by 3-6mg/kg in 3 divided doses ( Hb rises by

0.4g/day)0.4g/day)

For 6-8 wks after Hb is normalFor 6-8 wks after Hb is normal Iron products-Iron products-

Ferrous sulfateFerrous sulfate

Carbonyl iron(slow release)Carbonyl iron(slow release)


THERAPY OF I D ATHERAPY OF I D A

Parental iron therapy ( Iron in mg=wt in kgParental iron therapy ( Iron in mg=wt in kg×× Hb deficit in gm/dlHb deficit in gm/dl××4)4)

ProductsProducts

►►Iron dextran complexIron dextran complex

►►Ferric carboxy maltoseFerric carboxy maltose

non dextran IV carboxymaltose non dextran IV carboxymaltose

Indications for parenteral Indications for parenteral therapytherapy

Intolerance to oral ironIntolerance to oral ironMalabsorption Malabsorption Ongoing blood loss where oral Ongoing blood loss where oral

replacement can not match iron lossreplacement can not match iron loss

Reasons for non responseReasons for non response

Poor compliancePoor complianceAssociated B12/Folate deficiencyAssociated B12/Folate deficiency Interaction with drugs & dietInteraction with drugs & dietHemolytic anemiaHemolytic anemiaMalabsorption Malabsorption Enteric coated iron preparationsEnteric coated iron preparations Increasing on going blood loss.Increasing on going blood loss.


THERAPY OF I D ATHERAPY OF I D A Blood transfusion –rarely when Hb<4gm/dl, Blood transfusion –rarely when Hb<4gm/dl,

CCF, severe infection with poor iron CCF, severe infection with poor iron utilisationutilisation


PREVENTION OF I D APREVENTION OF I D A

Breast feeding and appropriate weaning Breast feeding and appropriate weaning dietdiet

Iron rich foodIron rich food Preterm and LBW babies-10-15 mg/day Preterm and LBW babies-10-15 mg/day

ironiron Iron supplementation during pubertyIron supplementation during puberty Increase ascorbic acidIncrease ascorbic acid

NUTRITIONAL ANEMIAS IN CHILDRENNUTRITIONAL ANEMIAS IN CHILDREN PREVENTION OF I D APREVENTION OF I D A

Decrease inhibitors Decrease inhibitors Salt fortification Salt fortification DewormingDeworming Foot wear useFoot wear use Safe drinking waterSafe drinking water


MEGALOBLASTIC ANEMIAMEGALOBLASTIC ANEMIA

INEFFECTIVE ERYTHROPOESISINEFFECTIVE ERYTHROPOESIS

DEFECTIVE SYNTHESIS OF DNADEFECTIVE SYNTHESIS OF DNA

INCREASED MCVINCREASED MCV

HYPERSEGMENTED NEUTROPHILSHYPERSEGMENTED NEUTROPHILS


CAUSES OF MEGALOBLASTIC ANEMIACAUSES OF MEGALOBLASTIC ANEMIA

FOLIC ACID DEFICIENCYFOLIC ACID DEFICIENCY

VITAMINB 12 DEFICIENCYVITAMINB 12 DEFICIENCY

MALNUTRITIONMALNUTRITION

INBORN ERRORS OF METABOLISMINBORN ERRORS OF METABOLISM


MEGALOBLASTIC ANEMIAMEGALOBLASTIC ANEMIA

FOLIC ACID DEFICIENCYFOLIC ACID DEFICIENCY

VITAMINB 12 DEFICIENCYVITAMINB 12 DEFICIENCY


FOLIC ACID DEFICIENCY ANEMIAFOLIC ACID DEFICIENCY ANEMIA

SOURCES OF FOLIC ACID:SOURCES OF FOLIC ACID:

-Green vegetables,fruits, -Green vegetables,fruits,

-Non veg liver,kidney-Non veg liver,kidney


FOLIC ACID DEFICIENCY ANEMIAFOLIC ACID DEFICIENCY ANEMIACAUSESCAUSESINADEQUATE FOLATE INTAKE(GOATS MILK)INADEQUATE FOLATE INTAKE(GOATS MILK)DECREASED FOLATE ABSORPTION(DRUGS)DECREASED FOLATE ABSORPTION(DRUGS)DEFECTIVE FOLATE METABOLISM-DEFECTIVE FOLATE METABOLISM- Congenital Dihydrofolate reductase Congenital Dihydrofolate reductase

deficiencydeficiency DRUG INDUCEDDRUG INDUCEDLAB DIAGNOSIS-P B S,RETIC COUNT, MCV >100fLLAB DIAGNOSIS-P B S,RETIC COUNT, MCV >100fL HYPER SEGMENTED NEUTROPHILSHYPER SEGMENTED NEUTROPHILS SERUM & R B C FOLATE LEVELSSERUM & R B C FOLATE LEVELS SERUM L D H SERUM L D H BM ERYTHROID HYPERPLASIABM ERYTHROID HYPERPLASIA


FOLIC ACID DEFICIENCY ANEMIA FOLIC ACID DEFICIENCY ANEMIA

CLINICAL FEATURESCLINICAL FEATURES

WEAKNESS,FATIGUE,IRRITABILITYWEAKNESS,FATIGUE,IRRITABILITY

PALLOR,GLOSSITIS,DIARRHOEA,PALLOR,GLOSSITIS,DIARRHOEA,

USUALLY ASSOCIATED WITH KWASHIORKAR AND USUALLY ASSOCIATED WITH KWASHIORKAR AND MARASMUS.MARASMUS.

..


THERAPY OF FOLIC ACID DEFICIENCY ANEMIATHERAPY OF FOLIC ACID DEFICIENCY ANEMIA

If diagnosis is established If diagnosis is established Folic acid 0.5mg-1.0mg/day oral/parenteralFolic acid 0.5mg-1.0mg/day oral/parenteral If diagnosis is in doubtIf diagnosis is in doubtFolic acid 0.1mg/day for 1wk as a dignostic test.Folic acid 0.1mg/day for 1wk as a dignostic test. Doses >0.1mg/day can correct anemia of B 12 Doses >0.1mg/day can correct anemia of B 12

deficiency but may aggrevate neurological signsdeficiency but may aggrevate neurological signs DURATION OF THERAPY:DURATION OF THERAPY: Folic acid 0.5mg-1.0mg/day for 3-4 wksFolic acid 0.5mg-1.0mg/day for 3-4 wks maintainance 0.2mg/daymaintainance 0.2mg/day


VIT B12 (COBALAMINE )DEFICIENCYVIT B12 (COBALAMINE )DEFICIENCY

CAUSES MEGALOBLASTIC ANEMIACAUSES MEGALOBLASTIC ANEMIA

HUMANS CAN NOT SYNTHESISE B12HUMANS CAN NOT SYNTHESISE B12

MAIN SOURCE IS NON VEG FOODMAIN SOURCE IS NON VEG FOOD


VITAMIN B12(COBALAMINE) DEFICIENCYVITAMIN B12(COBALAMINE) DEFICIENCY

METABOLISM OF B12METABOLISM OF B12

Ingestion- Cobalamine in FoodIngestion- Cobalamine in Food

Stomach-Cobalamine combines with R Protein&IFStomach-Cobalamine combines with R Protein&IF

Duodenum-Pancreatic proteases break R proteinDuodenum-Pancreatic proteases break R protein

Distal ileum-Cobalamine with IF is absorbed.Distal ileum-Cobalamine with IF is absorbed.

Plasma-Cobalamine binds to transport protein,TC II.Plasma-Cobalamine binds to transport protein,TC II.

In Cells- cobalamine enters cells by endocytosisIn Cells- cobalamine enters cells by endocytosis

Cobalamine is converted to Methyl cobalamine&Cobalamine is converted to Methyl cobalamine&

Adenosyl cobalamine which are important in Adenosyl cobalamine which are important in

DNA synthesisDNA synthesis


VIT B12(COBALAMINE) DEFICIENCY ANEMIAVIT B12(COBALAMINE) DEFICIENCY ANEMIA

CAUSESCAUSES

Inadequate intakeInadequate intake

Lack of Intrinsic Factor(I F )-congenital,juvenileLack of Intrinsic Factor(I F )-congenital,juvenile

Impaired absorptionImpaired absorption

Absence of vit B12 Transport Protein.Absence of vit B12 Transport Protein.


VIT B12(COBALAMINE) DEFICIENCY ANEMIAVIT B12(COBALAMINE) DEFICIENCY ANEMIA

CLINICAL FEATURESCLINICAL FEATURESWEAKNESS,FATIGUE,IRRITABILITYWEAKNESS,FATIGUE,IRRITABILITY

FTT,DEVELOPMENTAL DELAYFTT,DEVELOPMENTAL DELAY

PALLOR,GLOSSITIS,DIARRHOEAPALLOR,GLOSSITIS,DIARRHOEA

SENSORY DEFICITS,NEURO PSYCHIATRIC CHANGESSENSORY DEFICITS,NEURO PSYCHIATRIC CHANGES

ATAXIA,HYPOREFLEXIA,SEIZURES,BABINISKI’S ATAXIA,HYPOREFLEXIA,SEIZURES,BABINISKI’S

RESPONSERESPONSE

NEUROLOGICAL MANIFESTATIONS CAN OCCUR WITH NEUROLOGICAL MANIFESTATIONS CAN OCCUR WITH

OUT HEMATOLOGICAL MANIFESTATIONSOUT HEMATOLOGICAL MANIFESTATIONS..


VIT B12 DEFICIENCY ANEMIAVIT B12 DEFICIENCY ANEMIA LAB DIAGNOSISLAB DIAGNOSISHematological manifestations of folate &B12Hematological manifestations of folate &B12 deficiency are similardeficiency are similarMacrocytes ,ovalocytes,hypersegmented Macrocytes ,ovalocytes,hypersegmented

neutrophilsneutrophilsNeutropenia,ThrombocytopeniaNeutropenia,ThrombocytopeniaS.Vit B12 levels lowS.Vit B12 levels lowS.Methylmelonic acid,homocystein levels S.Methylmelonic acid,homocystein levels ↑↑ ↑↑ S.Iron &folic acid normal, S.Iron &folic acid normal, Serum LDH Serum LDH ↑↑ ↑↑ ↑↑ Urine Methylmelonic acid Urine Methylmelonic acid ↑ ↑ ↑↑ ↑ ↑Schilling test abnormal in pernicious anemiaSchilling test abnormal in pernicious anemia


VIT B12 DEFICIENCY ANEMIAVIT B12 DEFICIENCY ANEMIA

SCHILLING TESTSCHILLING TESTPatient ingests radio active vitaminPatient ingests radio active vitamin

After 2hrs pt receives 1mg of non radioactive vitamin After 2hrs pt receives 1mg of non radioactive vitamin

parenterallyparenterally

Normally 30% of radioactive vitamin is excreted in urine Normally 30% of radioactive vitamin is excreted in urine inin

24hrs24hrs

If radio active vitamin is <2% in urine it is abnormalIf radio active vitamin is <2% in urine it is abnormal

Test is abnormal even after therapy reversed the diseaseTest is abnormal even after therapy reversed the disease


TREATMENT OF B12 DEFICIENCY ANEMIATREATMENT OF B12 DEFICIENCY ANEMIA

VIT B12- 1mg parenterally gives prompt VIT B12- 1mg parenterally gives prompt responseresponse

If there is neurological involvement 1mg IM If there is neurological involvement 1mg IM dailydaily

for 2wksfor 2wks

Maitainance – 1mg IM once in a month life Maitainance – 1mg IM once in a month life long.long.


TO SUM UPTO SUM UPNUTRITIONAL ANEMIAS ARE TREATABLENUTRITIONAL ANEMIAS ARE TREATABLE

CAN BE CONTROLLABLECAN BE CONTROLLABLE

INTERVENTIONS ARE SIMPLEINTERVENTIONS ARE SIMPLE

INTERVENTIONS ARE AFFORDABLEINTERVENTIONS ARE AFFORDABLE

AFFORDABLE MEASURES ARE AVAILABLEAFFORDABLE MEASURES ARE AVAILABLE

Thank youThank you


IRON ABSORPTIONIRON ABSORPTION

SITE:DUODENUM& JEJUNUMSITE:DUODENUM& JEJUNUMFERRITIN: IRON ABSORBED BY MUCOSAL CELLSFERRITIN: IRON ABSORBED BY MUCOSAL CELLS BINDS TO A PROTEIN CALLED APOFERRITINBINDS TO A PROTEIN CALLED APOFERRITIN FORMS FERRITIN,(STORAGE FORM OF IRON)FORMS FERRITIN,(STORAGE FORM OF IRON)IRON IS STORED IN R E SYSTEM AS FERRITIN.IRON IS STORED IN R E SYSTEM AS FERRITIN.IRON ALSO STORED IN B M AS HEMOSIDERINIRON ALSO STORED IN B M AS HEMOSIDERINTRANSFERRIN-IRON COMBINED WITH IT IN PLASMATRANSFERRIN-IRON COMBINED WITH IT IN PLASMATRANSFERRITIN RECEPTORTRANSFERRITIN RECEPTOR


LAB DIAGNOSIS OF IDALAB DIAGNOSIS OF IDA Low HemoglobinLow Hemoglobin Low HematocritLow Hematocrit Low Mean Corpuscular VolumeLow Mean Corpuscular Volume Serum Ferritin <10ng/mlSerum Ferritin <10ng/ml Transferrin Saturation<15%Transferrin Saturation<15% TIBC>350TIBC>350µµg/dlg/dl Increased free erythrocyte Increased free erythrocyte

protoporphirynprotoporphiryn

Iron fortified food.Iron fortified food. Iron EDTA has been highly effective in Iron EDTA has been highly effective in

fortification trials with fortification trials with Egyptian flat breadsEgyptian flat breads, , curry powder in curry powder in South AfricaSouth Africa, , fish saucefish sauce in in ThailandThailand, and , and sugarsugar in in GuatemalaGuatemala. .

In In GrenadaGrenada , , flourflour used in commercial baking used in commercial baking is enriched with iron and B vitamins,. is enriched with iron and B vitamins,.

IndianIndian researchers have field tested with researchers have field tested with success iron fortified salt. success iron fortified salt.

Pasteurized milkPasteurized milk (iron 15 mg/ l and Vit. C 100 (iron 15 mg/ l and Vit. C 100 mg/l.)-Stekel 1986mg/l.)-Stekel 1986

Availability of dietary iron by Availability of dietary iron by cooking in cast iron utensils:cooking in cast iron utensils:

WHO 1992 prevalence of pregnancy anemia WHO 1992 prevalence of pregnancy anemia report, records that lowest, rates of all the report, records that lowest, rates of all the subregions of the developing world were subregions of the developing world were observed in observed in southern Africasouthern Africa, due to wide spread , due to wide spread use of iron cooking pots by indigenous people. use of iron cooking pots by indigenous people.

Agarwal et al (Lal et al IJMR-1973) had Agarwal et al (Lal et al IJMR-1973) had demonstrated that cooking in demonstrated that cooking in cast iron utensilscast iron utensils, , for boiling milk, cooking vegetables etc, for boiling milk, cooking vegetables etc, provided extra dietary iron. This available provided extra dietary iron. This available dietary iron is well absorbed.dietary iron is well absorbed.

Iron physiology and Iron physiology and metabolismmetabolism

Dietary sources of Iron can be classified Dietary sources of Iron can be classified as food sources and fortified foods.as food sources and fortified foods.

The amount of Iron varies widely between The amount of Iron varies widely between foods.foods.

Iron exists in food under two Iron exists in food under two forms, forms, heme and non heme iron. heme and non heme iron.

They are not only different in terms of They are not only different in terms of their sources, but also in terms of their sources, but also in terms of bioavailability.bioavailability.

Transfer of Iron to the Transfer of Iron to the circulation and transportcirculation and transport

Transferrin is the major protein Transferrin is the major protein responsible for transporting Iron in responsible for transporting Iron in the body.the body.

Transferrin receptors, located on the Transferrin receptors, located on the surface of nearly all cells in the body, surface of nearly all cells in the body, can bind two molecules of transferrin.can bind two molecules of transferrin.

Transferrin saturation is important in Transferrin saturation is important in assessing IDassessing ID..

Tissues with higher requirements of Iron Tissues with higher requirements of Iron (erythroid precursors, placenta and liver) (erythroid precursors, placenta and liver) contain higher transferrin receptors.contain higher transferrin receptors.

Once in tissues, Iron is stored as ferritin Once in tissues, Iron is stored as ferritin and hemosiderin compounds, which are and hemosiderin compounds, which are ppresent primarily in the liver, RE cells and resent primarily in the liver, RE cells and bone marrow.bone marrow.

The amount of ferritin in storage The amount of ferritin in storage compartment depends on Iron status compartment depends on Iron status which ranges from depleted to replete iron which ranges from depleted to replete iron statusstatus

Ferritin concentration expresses Body Iron Ferritin concentration expresses Body Iron Stores when assessing ID.Stores when assessing ID.

Host related factorsHost related factors

Iron stores and the amount of Iron stores and the amount of iron to which intestinal cells iron to which intestinal cells have been exposed constitute have been exposed constitute the main factors regulating iron the main factors regulating iron absorption.absorption.

Laboratory IndicesLaboratory Indices LAB DIAGNOSISLAB DIAGNOSIS Low HemoglobinLow Hemoglobin Low HematocritLow Hematocrit Low Mean Corpuscular VolumeLow Mean Corpuscular Volume Serum Ferritin <10ng/mlSerum Ferritin <10ng/ml Transferrin Saturation<15%Transferrin Saturation<15% TIBC>350TIBC>350µµg/dlg/dl Increased free erythrocyte Increased free erythrocyte

protoporphirynprotoporphiryn

TreatmentTreatment

THERAPY OF I D ATHERAPY OF I D A Treat underlying causeTreat underlying cause Oral iron therapyOral iron therapy

3-6mg/kg in 3 divided doses ( Hb rises by 3-6mg/kg in 3 divided doses ( Hb rises by 0.4g/day)0.4g/day)

Vit C, empty stomach or in between mealsVit C, empty stomach or in between meals For 6-8 wks after Hb is normalFor 6-8 wks after Hb is normal

Parental iron therapy ( Iron in mg=wt in Parental iron therapy ( Iron in mg=wt in kgkg×× Hb deficit Hb deficit××in gm/dlin gm/dl××4)4)

Blood transfusion –rarely when Blood transfusion –rarely when Hb<4gm/dl, CCF, severe infection with Hb<4gm/dl, CCF, severe infection with poor iron utilisationpoor iron utilisation

Response to treatmentResponse to treatment

Less irritable & increased appetite Less irritable & increased appetite within 24 hrswithin 24 hrs

Bone marrow response by 48 hrsBone marrow response by 48 hrs Increased reti count by 3Increased reti count by 3rdrd day day Increased Hb level by 2 monthsIncreased Hb level by 2 monthsBody iron store repletionBody iron store repletion


NUTRIENTS IN RBC DEVELOPMENTNUTRIENTS IN RBC DEVELOPMENT

PROTEINS-(METHIONINE DEFICIENCYPROTEINS-(METHIONINE DEFICIENCY LEADS TO DEFECTIVE DNA)LEADS TO DEFECTIVE DNA)IRONIRONVITAMIN- B12VITAMIN- B12FOLIC ACIDFOLIC ACIDVITAMIN CVITAMIN CVITAMIN AVITAMIN AVITAMIN B6VITAMIN B6VITAMIN B2VITAMIN B2OTHERSOTHERS

nutritional anemias in children.ppt

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childrenidadietary iron

enzymesnutritional anemias

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childreniron deficiency