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IRON DEFICIENCY ANAEMIA MBBSBDS IV.pptx
1. Iron deficiency
anaemia
DR ABBA AISHA MOHAMMED
DEPARTMENT OF HAEMATOLOGY
FACULTY OF BASIC CLINICAL SCIENCES
UNIVERSITY OF MAIDUGURI
7/10/2023
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2. OBJECTIVES
To define iron deficiency anaemia
To understand iron metabolism
To identify the causes & consequences of IDA
To be able to effectively diagnose and manage IDA
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3. OUTLINE
Introduction
Iron metabolism
Clinical features/ consequence of iron
deficiency/Stages of iron deficiency
Laboratory diagnosis
Treatment
Prevention
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4. INTRODUCTION
Iron deficiency is the decrease in total iron
content of the body
Iron deficiency anaemia occurs when iron
deficiency is severe enough to decrease/
halt erythropoiesis and cause development
of anaemia
IDA diminishes capability of individuals to
work and affects growth and learning
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5. CONT’D
Deficiency of iron is the most common cause of anaemia
globally
Affects >1.5 billion people worldwide
Occurs most frequently in under-developed countries
It is the most important differential diagnosis of”
microcytic hypochromic “anaemia (morphologic
classification)
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6. IRON METABOLOSM
o Iron requirements vary daily as it
compensates for losses from the
body and growth requirements
o Pregnant women, menstruating
females and adolescents have the
highest demands
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7. DAILY REQUIREMENTS OF IRON
Infants up to 4 months- 0.5mg
Infants 5-12 months and children-
1mg
Menstruating women-3mg
Pregnancy- 3-4mg
Adult male and postmenopausal
women-1mg
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8. SOURCES OF IRON
Animal sources- red meat, dairy
products(milk is a poor source
of iron)
Plant sources- fruits, cereals,
legumes,vegetables
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11. IRON METABOLISM
Dietary iron is present in foods in
the ferric form (ferric hydroxides and
ferric protein)
The proportion of iron absorbed
differs from one food to another;
meat is the richest source of iron
Depending on the type of food
taken, iron is absorbed partly as
haeme and partly as inorganic iron
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13. ABSORPTION OF IRON
Haeme iron is absorbed directly through
the duodenum to the portal circulation
While inorganic iron is first converted to
ferrous form (ferrireductase) and
internalized with the aid of DMT1
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14. CONT’D
Inside the cell it is either stored as ferritin
or transported to the plasma
Exit of iron from the duodenal enterocyte
into the portal plasma is controlled by
ferroportin
Ferrioxidase converts ferrous to ferric iron
to enable it bind to transferrin
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16. TRANSPORT OF IRON
Transferrin; a glycoprotein produce by the liver
delivers iron to tissues that have transferrin
receptors e.g marrow erythroblasts, for
incorporation into haemoglobin and other cells of
the body. Transferrin is then re-utilized
Iron in the erythroblast cytoplasm moves to the
mitochondria for haeme synthesis
Some iron is stored in the lysosome as ferritin
(sideroblasts)
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17. STORAGE OF IRON
Ferritin - water soluble consisting of a
protein shell and iron core, contains
numerous ferric oxyhydroxide molecules
and is readily mobilised for haemoglobin
synthesis when required
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18. CONT’D
Haemosiderin –represents aggregation of
ferritin from which most of the protein has
been removed. It is stored in the RES, it is
water insoluble and less readily available
for haemoglobin synthesis
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19. REGULATION OF IRON : HEPCIDIN
A 25 amino acid polypeptide hormone
produced by the liver
known to be the key regulator of iron
metabolism
It causes internalisation and degradation
of ferroportin; the only iron exporter at the
basolateral end of the enterocyte
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20. CONT’D
There by inhibiting iron absorption from
the GIT and release by the macrophages
Hepcidin levels fall in iron deficiency ,
hypoxia and erythropoietic drive
Plasma transferrin saturation and
inflammation stimulate hepcidin synthesis
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22. STAGES OF IRON DEFICIENCY
Iron store depletion- absent iron stores
Iron deficient erythropoiesis (latent iron
deficiency)- absent iron stores with
reduction of plasma concentration of
iron
Iron deficiency anaemia- the two above
with blood film features of iron
deficiency
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27. Clinical features
GENERAL FEATURES OF ANAEMIA-
Weakness, easy fatiguability, breathlessness
on exertion, tachycardia and a systolic heart
murmur e.t.c
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28. CONT’D
FEATURES RELATED TO IRON DEFICIENCY-
pica;abnormal intense desire to eat strange
substances such as clay,,paint cardboard etc.
atrophic glossitis, dysphagia,angular
stomatitis and koilonychia
Iron def. anaemia+ glossitis+dysphagia=
Patterson Kelly (or plummer-vinson)
syndrome
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29. Cont’d
FEATURES DUE TO UNDERLYING CAUSE-
bleeding from GIT,menorrhagia,alteration in
bowel habit, hemoptysis e.t.c
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32. DIAGNOSIS
1.PERIPHERAL BLOOD FILM
RED cells show Anisopoikilocytosis with
microcytic hypochromic cells, pencil cells,
occasional target cells
PLATELETS; thrombocytosis
LEUCOCYTES normal or increased (with
infection or infestation)
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33. CONT’D
NOTE: A dimorphic picture is seen if the
patient has received transfusion, has
coexisting folate or vit B12 deficiency or
received recent iron therapy
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35. CONT’D
5.TIBC/ Serum transferrin receptor ↑
6.Free red cell portopophyrin ↑
7.Serum hepcidin ↓
8.Bone marrow examination (GOLD
STARNDARD ) stained with Prussian blue
(perl’s reaction) will show absent iron in
macrophages, but is not necessary except in
complicated cases
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39. TREATMENT
1. Identify the underlying cause and treat
appropriately
2. Iron replacement therapy
Aim- to correct anaemia and replenish the
stores
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40. CONT’D
Two forms of iron replacement therapy
are in use
1. The oral formulations
2. The parenteral formulations
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41. CONT’D
1.Ferrous sulphate (BEST preparation) ,
contains 67mg of elemental iron in 200mg
tablet. Administration is 6-8hrly on an empty
stomach. Side effects include nausea,
abdominal discomfort and diarrhea or
constipation
2. Ferrous gluconate , contaims 37mg iron in
300mg tablet(does not deliver required iron
content) ,has less side effect
3. Ferrous fumarate
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42. CONT’D
NOTE: Therapy is given for at least 6 months
to correct anaemia and replenish the stores
Failure to respond to oral iron therapy-
On going haemorrhage
Non-compliance
Wrong diagnosis
Mixed deficiencies
Malabsorption
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43. CONT’D
PARENTERAL IRON THERAPY –
1. Ferric-hydroxide sucrose
2. Iron dextran
3. Ferric carboxymaltose
These are calculated according to weight and
degree of anaemia
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44. CONT’D
1 and 2 are commonly used in our
centre
1 is give as an slow IV injection or
infusion
2 is given as deep IM injection spread
over a week
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45. CONT’D
Indicated only – GI bleeding, severe
menorrhagia, chronic haemodialysis,
erythropoeitin therapy and when oral iron
is ineffective
Side effects of parenteral iron therapy
includes- hypersensitivity reactions, muscle
staining,
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46. CONT’D
NOTE: there is no superiority in
haematological response of parenteral iron
over oral iron therapy
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47. PREVENTION
Iron supplementation
Food fortification
Dietary modification
Control of viral. Bacterial and
parasitic infections
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48. SUMMARY
Iron deficiency anaemia is a significant
public health problem globally with varied
aetiology ranging from loss of iron via
blood loss to inadequate intake and
problems of metabolism
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49. CONT’D
Women tend to have substantially lower iron
stores than men, thus are more vulnerable to
iron deficiency when iron intake is lowered or
need increases
Diagnosis is made using PBF ,red cell indices in
addition to evaluation of iron stores
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50. CONT’D
Treatment is aimed at correcting anaemia
and replenishing the stores
Prevention is by nutrirional education and
supplementation in diets
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52. REFERENCES
New concepts in iron deficiency anaemia.
British journal of General practice 2017
Camaschella C. New insights into iron
deficiency and iron deficiency anaemia.
Blood Rev.2017
Williams Hematology 9th Edition
Postgraduate Haematology 7 Edition A. V.
Hoffbrand
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53. QUIZ 5 minutes
One of your senior colleagues that took
part in the just concluded examination
in laboratory medicine and
pharmacology was excited by the
outcome and invited you for an outing
where you ate bread , suya and drank a
cup of tea. What is wrong with such a
combination? What is the
pathophysiology of the attendant
problem ?
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