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FACTORS AFFECTING SKIN COLOR HEMOGLOBIN CONCENTRATION STATE OF CONSTRICTION DILATATION OF PERIPHERAL VESSELS PIGMENTATION AND SCT FLUID

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FACTORS AFFECTING SKIN COLOR

HEMOGLOBIN CONCENTRATION

STATE OF CONSTRICTION

DILATATION OF PERIPHERAL VESSELS

PIGMENTATION AND SCT FLUID

ANEMIA REDUCTION IN RED CELL MASS

REDUCTION IN BLOOD HEMOGLOBIN CONCENTRATION

FUNCTION OF THERED CELL

TO DELIVER AND RELEASE ADEQUATE QUANTITIES OF OXYGEN TO THE TISSUES TO MEET THEIR METABOLIC DEMANDS

CRITERIA FOR IDENTIFYING CHILDREN WITH LOW HgB & HCT

VALUESAGE Hgb(g/dl) Hct (%) 6-23 MOS < 10 < 312-5 YRS < 11 <346-12 YRS < 12 < 37

HEMOGLOBIN LEVELAND SYMPTOMS

Hgb ( g ) SYMPTOMS 9 – 11 little to no dysfunction 5 – 7 exertional dyspnea 6 . 0 some weakness 3 . 0 dyspnea at rest 2 - 2.5 cardiac failure

EVALUATION OF THEANEMIC PATIENT

HISTORY

PHYSICAL EXAMINATION

LABORATORY TESTS CBC RBC INDICES RETICULOCYTE COUNT EXAMINATION OF THE PERIPHERAL SMEAR

RED BLOOD CELLINDICES

MCV = VOLUME OF PRC (hct) ___________________ X 1000 RBC COUNT

NV = 80 - 100 fl

RED BLOOD CELLINDICES

MCH = Hgb -------- RBC COUNT NV = 27 – 34 pg

RED BLOOD CELLINDICES

MCHC = Hgb --------- VOLUME OF PRC

NV = 32 – 36 %

CORRECTED RC ORRETICULOCYTE INDEX

ACTUAL HCT X OBSERVED RC ----------------------- ( % ) DESIRED HCT

NV = 1 – 1.5 %

RETICULOCYTOSIS ACUTE BLOOD LOSS

HEMOLYTIC ANEMIA

AFTER A THERAPEUTIC TRIAL OF IRON

RETICULOCYTOPENIA BONE MARROW FAILURE

APLASTIC ANEMIA

LEUKEMIA

PERIPHERAL SMEAR HYPOCHROMIA , MICROCYTOSIS , ANISOPOIKILOCYTOSIS , TARGET CELLS , THROMBOCYTOSIS , THROMBOCYTOPENIA

CHEMICAL STUDIES DECREASED SERUM IRON INCREASED TOTAL IRON – BINDING CAPACITY TRANSFERRIN SATURATION IS BELOW 15 % SERUM IRON BELOW 5O ug / dl

CLASSIFICATION OF ANEMIA ACCORDING TOFUNCTIONAL DISTURBANCES

1.DISORDERS OF EFFECTIVE RC PRODUCTION

2. DISORDERS WITH RAPID ERYTHROCYTE

DESTRUCTION OR RC LOSS

DISORDERS OF EFFECTIVERC PRODUCTION

DEPRESSED NET RATE OF RC PRODUCTION DISORDERS OF ERYTHROCYTE MATURATION INEFFECTUAL ERYTHROPOIESIS ABSOLUTE FAILURE OF ERYTHROPOIESIS

ANEMIA

INIT

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TIV

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DIA

GN

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CO

NF

IRM

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IRS

AD

DIT

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TU

DIE

SRED CELL INDICES

MCV, MCHC, MCH, RDW, HDW

PERIPHERAL SMEAR

RETICULOCYTE COUNT AND INDICES

DIRECT ANTI GLOBULIN TEST

G6PD screening test Osmotic

fragility

Hb ISOELECTROFOCUS

ING & OTHER TESTS FOR

RARE Hb VARIANTS

HISTORYPHYSICEL EXAMINATIONNON-HEMATOLOGICAL

DISEASES:(Renal, Thyroid, Metabolic,

Others)

HbELECTROPHO

RESISBone MarrowAspirate/Blopsy

Test for unstable Hbs

CYTOGENETIC STUDIES

Indirect bilirubinLDH, Heptogloblin,Serum B12Serum, RBC FolateSerum ferritin, iron,TIBCCirculating transferrinReceptorSerum Lead and RBC ZPP

RBC Enzyme Panel

Membrane protein studies

IRON DEFICIENCYANEMIA

MOST COMMON CAUSE OF ANEMIA COMMON IN AGES 6 – 24 MONTHS

FORMS OF IRONACCORDING TO ITS

STABLE OXIDATIVE STATES

FERROUS ( Fe 2+ )

FERRIC ( Fe 3+ )

IRON – BINDINGAGENTS (CHELATORS)

DESFERRIOXAMINE

TRANSFRRRIN

DISTRIBUTION OF IRON AVERAGE ADULT - 3 - 5 g ( BALANCE = DIETARY UPTAKE AND LOSS ) LOSSES : SKIN - 1 mg/ day MENSTRUATION - 2 mg /day

ETIOLOGY OF IRONDEFICIENCY

A. INADEQUATE SUPPLY OF IRON 1 . LACK OF IRON STORES AT BIRTH

( LBW ,PT , TWIN OR MULTIPLE BIRTHS , SEVERE

IDA IN MOTHER , FETAL BLD LOSS ,

BLEEDING FROM THE 1ST FEW DAYS OF LIFE ) 2. INADEQUATE INTAKE-DEFICIENT DIETARY IRON

ETIOLOGY OF IRON DEFICIENCY

B . IMPAIRED ABSORPTION 1. CHRONIC OR RECURRENT DIARRHEA 2. MALABSORPTON SYNDROME 3 . GASTROINTESTINAL ABNORMALITIES

ETIOLOGY OF IRONDEFICIENCY ANEMIA

C. EXCESSIVE DEMANDS FOR IRON FOR GROWTH AS SEEN IN PT , LBW , INFANTS , ADOLESCENT AND PREGNANCY

ETIOLOGY OF IRON DEFICIENCY ANEMIA

D . BLOOD LOSS

1. ACUTE OR CHRONIC HEMORRHAGE

2 . PARASITIC INFECTION (HOOKWORM TRICHURIS trichiura )

FACTORS THAT MODIFYIRON ABSORPTION

PHYSICAL STATE ( BIOAVAILABILITY ) HEME > Fe 2+ > Fe 3 + INHIBITORS PHYTATES , TANNINS , SOIL , LAUNDRY STARCH , IRON OVERLOAD COMPETITORS COBALT, LEAD , STRONTIUM FACILITATORS ASCORBATE, CITRATE , AMINO ACIDS

ROLE OF IRON DNA SYNTHESIS

HOST OF METABOLIC PROCESSESS

CONSEQUENCES OFIRON DEFICIENCY ANEMIA

1. ANEMIA 2 . GROWTH AND DEVELOPMENTAL RETARDATION 3 . EPITHELIAL CHANGES 4 . MISCELLANEOUS.

STAGES OF IRON DEFICIENCY

1 . PRELATENT IRON DEFICIENCY

2. LATENT IRON DEFICIENCY

3. FRANK IRON DEFICIENCY

STAGES OF IRON DEFICIENCY

PRELATENT IRON DEFICIENCY

DEPLETED STORES WITHOUT A CHANGE IN HCT OR SERUM IRON LEVELS RARELY DETECTED

STAGES OF IRON DEFICIENCY

LATENT IRON DEFICIENCY DECREASED SERUM IRON LEVEL TOTAL IRON - BINDING CAPACITY INCREASES WITHOUT A CHANGE IN THE HCT DECREASED TRANSFERRIN SATURATION

STAGES OF IRON DEFICIENCY

IRON DEFICIENCY ANEMIA

ASSOCIATED WITH ERYTHROCYTE MICROCYTOSIS AND HYPOCHROMIA

EFFECTS OF IRON DEFICIENCY

ANEMIA

GROWTH AND DEVELOPMENTAL RETARDATION EPITHELIAL CHANGES

MISCELLANEOUS

EFFECTS OF IRONDEFICIENCY

ANEMIA IMPAIRS TISSUE OXYGEN WEAKNESS , FATIGUE , PALPITATIONS AND LIGHTHEADEDNESS REACTIVE THROMBOCYTOSIS

EFFECTS OF IRONDEFICIENCY

GROWTH AND DEVELOPMENT GROWTH AND DEVELOPMENTAL ABNORMALITIES IMPAIRS NEUROLOGIC FUNCTIONS ( BEHAVIORAL ABNORMALITIES , MOTOR INCOORDINATION AND SEIZURE )

EFFECTS OF IRONDEFICIENCY

EPITHELIAL CHANGES ANGULAR STOMATITIS ,GLOSSITIS , FLATTENED AND ATROPHIC LINGUAL PAPILLAE , PLUMMER- VINSON ( FORMATION OF POSTCRICOID ESOPHAGEAL WEB ) , KOILONYCHIA OR SPOONING OF THE FINGERNAILS

EFFECTS OF IRON DEFICIENCY

MISCELLANEOUS PICA ( CONSUME LAUNDRY STARCH, ICE AND SOIL CLAY ) MASSIVE HEPATOSPLENOMEGALY , POOR WOUND HEALING AND BLEEDING DIATHESIS ZINC DEFICIENCY LEAD INTOXICATION PSEUDOTUMOR CEREBRI

DIAGNOSIS IN INFANTS : HIGH INDEX OF SUSPICION 1. PREMATURITY 2 . BLOOD LOSS 3 . FED EXCLUSIVELY ON MILK 4 . CHRONIC DIARRHEA

PREVENTION 1. ADMINISTRATION OF IRON TO EXPECTANT MOTHERS 2. EARLY INTRODUCTION OF SOLID FOOD 3 . SUPPLEMENTAL IRON : 1O – 15 MG OF ELEMENTAL IRON / DAY ( 6 -8 WKS OF AGE )

TREATMENT OF IRONDEFICIENCY ANEMIA

DETERMINE THE CAUSE

CORRECT THE ABNORMALITY

SPECIFIC TREATMENTOF IRON DEFICIENCY

ANEMIA 1. ORAL SUPPLEMENTATION

2. PARENTHERAL IRON REPLACE MENT

TREATMENT( ORAL IRON )

ORAL FERROUS SULFATE : 6 MG / KG / DAY ( 6 – 8 WKS AFTER NORMAL HGB VALUE IS ATTAINRD ) OLDER CHILDREN : 1OO – 2OO MG / DAY OF ELEMENTAL IRON

POOR RESPONSETO ORAL IRON

NONCOMPLIANCE ONGOING BLOOD LOSS INSUFFICIENT DURATION OF THERAPY HIGH GASTRIC pH INHIBITORS OF IRON ABSORPTION / UTILIZATION INCORRECT DIAGNOSIS

INHIBITORS OF IRONABSORPTION

LEAD INTOXICATION ALUMINUM INTOXICATION (HEMODIALYSIS )

CHRONIC INFLAMMATION NEOPLASIA

PARENTHERAL IRONREPLACEMENT

INDICATIONS

1. POORLY TOLERATED ORAL IRON

2 RAPID REPLACEMENT IRON STORES

3. GI IRON ABSORPTION IS COMPROMISED

IRON DEXTRAN ADMINISTERED BY IM OR IV ROUTE “ Z- TRACK “ INJECTION TO MINIMIZE SC LEAK 10 -15 % - TRANSIENT ARTHRALGIA RETICULOCYTOSIS IN IO DAYS COMPLETE CORRECTION IN 3 -4 WKS

TREATMENT( BLOOD TRANFUSION )

INDICATION : SEVERE ANEMIA

DEBILITATED FROM INFECTION

SIGNS OF CARDIAC DECOMPENSATION

EFFECT ON THE FETUSOF MATERNAL IRON

DEFICIENCY “ MATERNAL IRON STATUS DETERMINES THE IRON STORES OF THE NEONATE . “

" AN OUNZE OF PREVENTION IS BETTER THAN A POUND OF CURE . "

SYSTEMIC DEFECTSIN IRON DEFICIENCY

ANEMIA OF CHRONIC INFLAMMATION :

1. INEFFECTIVE IRON UTILIZATION

2. LOW PLASMA ERYTHROPOIETIN LEVELS

CONSEQUENCES OF IRONOVERLOAD

1. HEART

2. LIVER

3. ENDOCRINE