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Lecture 2 Assist. Prof Dr. Hussein NajiAl-Shammari
Hypochromicanaemiaand|ronDeficiencyAnemia,
lron Deficiency is the most common cause of anaemia world wilde. lt is the most
common cause of microcytic hypochromic anemia (Low MCV,MCHC, MCH). lron
deficiency is the most common micronutrient deficiency in the world affecting 24o/o of lhe
world population. This is because iron has limited capacity for absorption and excess loss
from hemorrhage.
lron Distribution in the bo
Site Male q female Percentaqe of total
Hb (circulatino) 2.4 1.7 65o/o
FerriUHemosid (storage)
Liver, bone manow, spleen
0.3-1.5 0.2-1.0 30o/o
mvoolobin 0.15 0.12 3.5o/o
Enzvmes 0.02 0.015 O.5o/o
Transferrin bound iron
(plasma)
0.004 0.003 0.1o/o
Total 3-5 q 2-3 q
DIETARY IRON:
The averaqe diet contains 10-1Smq iron from which 5-1Oyo absorbed (1-
1.5mq/davl
There are 2 types of iron in the diet; haem iron and non-haem iron
Haem iron is present in Hb , muscle meat, and liver.
Non-haem iron is obtained from cereals, vegetables & beans
Milk is a poor source of iron, hence breast-fed babies need iron supplements
RISK GROUPS for iron deficiency:
1. Infants , Under 5 children, Children of school age both sex,
2. Adolescent girls.
3. Women of child bearing age (pregnant and lactation).
STORAGE OF IRON
iron is stored as fenitin & hemosiderin compounds.
1. Ferritin: water soluble protein-iron complex in tissue and plasma. Ferritin level reflects
amount of stored iron in the body & is important in assessing iron deficiency
2. Hemosiderin: insoluble protein-iron complex as storage iron, visible in macrophages
after staining by Perls (Prussian blue) reaction.
/)t

Dailv lron requirmenl s

Lossby; GlT, UT,
Skin. hair loss
Growth mense pregnancy total
children 0.5 0.5 1.0
female 12-15 vear 0.5 -1 0.5 0.5-1 1.6-2.5
menstruation 0.5-1 00 0.5-1 1-2
preqnancy 0.5-1 00 1-2 1.5-3
postmenopausal 0.5-1 00 0.5-1
Adult male 0.5-1 00 0.5-1
Factors favoure Factors recluclno absorptlon
Hem iron Inoroanie rron
Ferrous iron Fe2* Fenic iron Fe3+
Acids:Hcl. vitamin C Alkalis : antlacids , pancreatic secrtion
Sugar, aminoacids Precioit. aqents: phvtate, phosphate
lron deficiencv iron execess
pregnancy Decreae erythropoiesis
evthroooisis infection
tea
lron loss : 1 mg of iron is lost each day usually balanced by dialy absorbtion
h'on absorbtion ls restricted to the needs of the body:
Main si{es ofahsorttion are; Duadenum, Upperieiunum
Transport of iron
Transfenin Transferrin is the major protein responsible for transporting iron in the
body, can bind two IRON atoms . lt is produced in liver cells with increased
synthesis in iron deficiency
T.otal iron bindirlg.c.Apqcity fl-lBC): only 113 of transfenin saturated with iron
Plasma Transfenin : 300 ptgldl and Plasma lron: 60-180 ;tg/dl
Causes of iron deficiencyETlO LOGY:
1. Chronic blood loss : Menonhagia, GIT hemorrhagia, Bleeding disorder, Pulmonary
lesions with bleeding, Hemodialysis, Hematuria (chronic), Frequent blood venisection
and donation (250 mg ircn /unit blood).
2. Increased demand : Pregnancy, Lactation, Rapid growth
3. Malabsorbtion of iron (diseae of absorbtion sites) .
4. Inadequate iron intake: Decreased iron in the diet, Vegetarianism
5. Pica
,,i . '

The steps of iron deficiency (developments) .

Continue negative iron balance... .Depletion of iron siores-. . ... Reduction serum Fer1tin
and iron......Reduction in Hb syntherir,....' red cells changes asAnaemia of hypochromia'
microcytic with Pencil shaPe RBC.
c. Sideroblastic anemia
d. Anemia of chronic diseases , late stages
e. Lead poisoning
ic anaemia Labo
Laboratorv diaqnois of IDA ( Features):
A._ Hematolosv:
1. Low HbJrtc,RBC: MCV,MCH,MCHC:
2. Low Retics count.
3. Plt: High/ normal
4. WBC:Normal.
5. Smear (blood film): Hypochromia,anisocytosis,microcytosis' poikilocytosis' pencil
cells.
8.. Eigchemic.a/ chaEoes
1. Serum tron: + ltttormal value : 60 - 180 pgldL)
2. TIBC: t lt tormat value 250 ' 430 ptg/dL)
3. Serum Ferritin J (ru : Female;10-tSO pg/1, Male;29-248 pg/L)
4. Transfenin saturation (Fe/TlBd normai i tSq6): (<15% indicate IDA)
5. Serum Transfenin RecePtor: t
C. Bone narrcw :,
Erythroid hyperplasia, micronormoblastic maturation, with ragged cytoplasm
absence of haemoglobin'
a. lron deficiencY anemia
b. Thalassemia.
faa*rrrac af lrrrn llaficie Anaemia anc other hpochrom
Type of hyPochromic
anaemia
IDA Thalassaemi
a
Chronic diseases Sideroblastic
low N/R L ?/ high aquir. MCV low
MCH low lnw
reduced hiqh S. iron low Norrna/nton
reduced normal TIBC raised normal
N/Low
N/ raised
r9!r9l-- - raised S Trensf receotor raised variable
s. ferritin low Normallhigh present Bone stores absent oresent oresenl
ervthroblast absent present absent Rinq forms
Hb ElectroPhor. normal A2lFIothers normal normal

Ifie #iR,gno,€.trg prllcedure iF rlof cornnfete uqfif ffie $qr'{er{'vin$ p'Ff4ofgqy is

disglose4
Treatment:
1. Treatment of undeling cause '
2. Replace iron and treat underlying disease'
3. Response can be followed ny reiic. increase in 1-2 weeks .
4. Hb be nrrnal al 2-4 months
5. Replacement therapy for 6-12 months to reptenish stores of iron
that For an individual to become iron deflcient, a prolonged period (approximately 6
vears), of negative iron balance is required'
Causes of treatment failure
1. Incorrect diagnosis
2. Complicating illness
3. Inadequate PrescriPtion
4. Continuing loss / malabsorption
5. Non comPliance


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