Group E presented on iron deficiency anemia. Key points include: 1. Iron is essential for hemoglobin production but 10% of ingested iron is absorbed. 2. Iron deficiency anemia results from negative iron balance and is characterized by microcytic, hypochromic anemia. 3. Treatment involves identifying the underlying cause, such as blood loss, and correcting the deficiency with oral or parental iron supplements.

1. IRON DEFICIENCY
ANEMIA
GROUP E

2. GROUP E MEMBERS
• DUNMADE DEMILADE CHS/016/16778
• JONES-ERUE JEVAOGHENE CHS/016/17026
• ADEWARA OLUWADAMILOLA CHS/017/17922
• OLOTU ADEMOLA ADELEKE CHS/015/15523
• ACHILE ESTHER CHS/016/16994

3. IRON
• It is a mineral that the body needs for growth and
development. For example, The body needs iron
to make hemoglobin and myoglobin
• It is the 2nd most abundant metal in earth’s crust
• Most common nutritional deficiency in the world
• Still only 10% ingested Fe is absorbed by
humans

4. • The body needs the right amount of iron.
• Too little amount of iron in the blood causes iron
deficiency anemia while
• Too much iron in the blood can lead to food
poisoning.
• Some people have a inherited disease called
hemochromatosis which causes too much iron to
build up in the body.

5. Iron is essential for many metabolic processes. It
has:
• the ability to exist in more than one relatively
stable oxidation state which are both
• ferric(Fe3+) and
• ferrous(Fe2+) forms
• the ability to form many complexes.

6. DISTRIBUTION OF BODY IRON
• The concentration of iron in the adult human body
is normally about 50 mg/kg in males and 40
mg/kg in females.
• 450mls of whole blood contains 200mg of iron
• Iron is found in the following proteins
1. Haemoglobin (65%)
2. Ferritin and haemosiderin (30%)
3. Myoglobin (3.5%)
4. Haem enzymes (Cytochromes b, a and c
as well as in the cytochrome P450
enzymes) 0.5%
5. Transferrin bound iron (0.1%)

7. HEMOGLOBIN Hemoglobin
contains heme
and globin,
Heme is a
porphyrin ring
containing an
iron atom
Each
hemoglobin
molecule can
bind 4 oxygen
molecules at

8. FERRITIN
• Ferritin is the primary iron storage protein which
provides a reserve of iron.
• It is a multi subunit protein
• It is primarily intracellular how ever some may be
found in plasma

9. HAEMOSIDERIN
• Haemosiderin is a water-insoluble crystalline,
protein–iron complex, visible by light microscopy
when stained by the Prussian blue (Perls’)
reaction. Haemosiderin is predominantly found in
macrophages rather than hepatocytes.
• It is a long term iron storage pool

10. TRANSFERRIN
• Transferrin is a single chain polypeptide
present in plasma (1.8–2.6 g/L) and
extravascular fluid .
• The protein is synthesized predominantly by
the liver into the blood, synthesis being
inversely related to iron stores ad is secreted
into the blood.
• Two atoms of ferric iron bind to each molecule.
• It transports iron through the blood to various
tissues such as spleen, bone marrow e.t.c
• Transferrin carries less than 1% of total body
iron

11. IRON ABSORPTION AND EXCRETION
• Iron absorption depends not only on the amount
of iron in the diet, but also on the bioavailability of
that iron
• In a normal diet, there is approximately 10 –
25mg of iron supply daily
• But, only about 1mg of this is usually absorbed
per day
• Most dietary iron is nonheme form, but is not
absorbed as readily as heme iron

12. PATHWAYS OF IRON ABSORPTION
• There are 2 pathways of iron absorption depending on the
organicity;
• Iron absorption occurs mainly in the epithelial cells lining the villi
close to the gastroduodenal junction
• The 1st pathway involves inorganic (non heme) iron which
accounts for the majority of the iron in plants
• The 2nd pathway invovles organic (heme) iron which is
present mainly in meat, poultry and fish

14. ABSORPTION OF INORGANIC IRON
• At physiological pH, inorganic iron exists in the
oxidized, ferric (Fe3+) state.
• To be absorbed, iron must be in the ferrous
(Fe2+) state or bound by a protein such as heme.
• The low pH of gastric acid in the proximal
duodenum allows a ferric reductase enzyme,
duodenal cytochrome B (Dcytb), on the brush
border of the enterocytes to convert the insoluble
ferric (Fe3+) to absorbable ferrous (Fe2+) ions.

15. • Once ferric iron is reduced to ferrous iron in the
intestinal lumen, a protein on the membrane of
enterocytes called divalent metal cation
transporter 1 (DMT1) transports iron across the
membrane and into the enterocyte.
• For heme iron, it is absorbed directly through the
help of the heme transporter into the enterocyte
where it is enters the labile pool.

16. • Once inside the enterocyte, some of the iron is
incorporated as mucosal ferritin
• Iron for retention by the body is transported into
the plasma via ferroportin-1 in the basolateral
membrane
• Before absorption into the plasma, The iron is
first converted from Fe2+ to Fe3+ by
hephaestin which is found in the villous cells of
the small intestine

18. REGULATION OF IRON ABSORPTION
• Iron absorption may be regulated at;
I. Stage of mucosal uptake
II. Stage of transfer into the blood
• The regulation is through a peptide called
hepcidin

19. HEPCIDIN
• It is a small peptide of 20-25 amino acids and it is
predominantly expressed in the liver
• It is a negative regulator of iron absorption,
transport and release from macrophages
• It also accelerates the destruction of iron
• Hepcidin is decreased in Iron deficiency, hypoxia
and ineffective erythropoiesis
• it is increased in increased iron stores and
inflammation

20. MECHANISM OF ACTION OF HEPCIDIN
• It binds to cell-surface ferroportin resulting in the
internalization and degradation.
• This leads to sequestration of iron within the cells

21. IRON EXCRETION
• Iron is closely conserved in humans
• <0.05% of iron is lost per day normally
1. Very small amounts in urine, bile and sweat
2. Cells shed from skin, intestinal and urinary
tracts
3. Menstrual blood loss
Humans have NO other physiologic means to
excrete excess iron

22. INTRODUCTION TO IRON DEFICIENCY
ANEMIA
• Most common form of anaemia in the world.
• Most important cause of microcytic, hypochromic
anaemia.
• Usually a result of negative iron balance (Loss >
Gain)

23. STAGES
There are 3 stages in the development of Iron
deficiency anaemia:
1. Pre latent stage:
• Begins when there is a negative iron balance.
• Iron stores reduced.
• Serum iron levels normal.
• No symptoms.

24. 2. Latent stage
• Stage of iron depleted erythropoiesis
• Iron stores depleted
• Iron absorption increases
3. Iron Deficiency Anaemia
• Iron stores depleted
• Serum Transferrin saturation falls

26. MCV HB Fe
ABSORPTION
Tf
SATURATION
sFRTN MARROW
IRON
TIBC
PRE-LATENT N N N
LATENT N N ↑ ↓ ↓ Absent ↑
FRANK IDA ↓ ↓ ↑ ↓ ↓ Absent ↑
↓
↑ ↓

27. CAUSES OF IRON DEFICIENCY
• Chronic blood loss, especially uterine or from
the GIT , is the dominant cause in the western
world
• Blood loss from the GIT could be due to;
• Peptic ulcer disease
• Gastric carcinoma
• Hemorragic gastritis
• Hemorrhoids
• Colonic carcinoma
• Cow’s milk intolerance in infants

28. • Dietary deficiency, is a common cause in the
developing world
• Pregnancy
• Prematurity
• Impaired absorption
• Hookworm infestation

29. OTHER CAUSES OF IRON DEFICIENCY

31. GENETIC CAUSES
• Mutations in the gene encoding DMT1,
glutaredoxin 5
• Hypotransferrinaemia or atransferrinaemia
• Deficiency of ceruloplasmin
• Iron refactory iron deficiency anaemia.

32. Certain groups of people are at risk of developing
IDA
• Pregnant women
• Premenopausal women
• Infants
• Adolescents

33. CLINICAL FEATURES
• Generally, there is
• Pallor
• Fatigability
• Weakness
• Dizziness
• Irritability

34. CLINICAL FEATURES
• Koilonychias (ridged nails,breaking easily),
• Angular stomatitis
• Painless Glossitis
• Pharyngeal webs and dysphagia (Paterson- Kelly
syndrome)

35. ANGULAR STOMATITIS

36. KOILONYCHIAS(SPOON NAILS)

37. CLINICAL FEATURES
• Hair loss
• Partial villous atrophy, with minor degrees of
malabsorption of xylose and fat, reversible by iron
therapy
• Blue sclera
• Pica(unusual dietary cravings)

38. • Infants with iron deficiency anaemia may have
impaired mental development and function
• Premature labour is more frequent in mothers
with iron deficiency. Iron deficiency anaemia
could also be a cause of pruritus

39. LAB. FINDINGS IN IRON DEFICIENCY
ANEMIA
• MCV is reduced to 50 to 60 fl (where the normal
value is 80 to 100 fl).
• MCH is reduced to 15 to 20 pg (where the
normal value is 27 to 33 pg).
• MCHC is reduced to 20 to 25 g/dl (where the
normal value is 30 to 35 g/dl).
• Reduced Haemoglobin
• Increased platelets
• Normal WBC; except in hookworm infections

42. BONE MARROW
• Hypercellularity
• Mild to moderate erythroid hyperplasia, and this is
polychromatic
• Micro-normoblasts are seen- pyknotic nuclei with
ragged cytoplasm
• The iron stain of bone marrow shows the
absence of stainable iron from stores and
developing erytgroblasts

43. SERUM IRON AND TOTAL IRON BINDING CAPACITY(TIBC)
• Serum iron is reduced
• TIBC is increased and could even be less than 10% saturated.
SERUM TRANSFERRIN RECEPTOR AND SERUM FERRITIN
• Serum transferrin receptor is increased in iron deficiency
anemia
• Serum ferritin level is very low in iron deficiency anemia

44. SERUM FERRITIN LEVEL
• Serum ferritin is the most commonly employed indicator of the
size of iron stores
• Serum ferritin level <15g/L IS DIAGNOSTIC OF IRON
DEFICIENCY ANEMIA
• Serum ferritin level of 15-30g/L IS SUGGESTIVE OF IDA

45. • Ferritin which is an acute phase protein is also raised in
1. Liver disease
2. Malignancy
3. Inflammation
4. Infection

46. MANAGEMENT
• Identification and treatment of the underlying
cause.
• Correction of deficiency by therapy with inorganic
iron.
• Iron may be administered in one of several forms:
• -Orally, as simple iron salts
• -Parenterally, as an iron-carbohydrate complex
• For the therapy of iron deficiency in adults, the
dosage should be sufficient to provide between
100 and 200 mg elemental iron daily

47. •Preparations of oral iron include;
a) Ferrous sulphate which contains 67mg of
elemental iron per 200mg
b) Ferrous gluconate which contains 37mg of
elemental iron per 300mg
Iron is absorbed more completely when the
stomach is empty
It is necessary to continue treatment for 3 - 6
months after the anemia is relieved
ORAL IRON THERAPY

48. • SIDE EFFECTS:
• Heartburn,
• Nausea
• Abdominal cramps
• FAILURE OF ORAL IRON THERAPY can be
caused:
• Malabsorption of iron
• Inadequate prescription (dose or form)
• Incorrect diagnosis
• Noncompliance of the patient.

49. PARENTERAL IRON THERAPY
• Is indicated when the patient
a) Demonstrates intolerance to oral iron
b) Loses iron (blood) at a rate too rapid for the oral intake
c) Has a disorder of gastrointestinal tract
d) Is unable to absorb iron from gastrointestinal tract
• Parental Preparations include
1. Iron - dextran
2. Iron sucrose
3. Iron carboxymaltose
4. Iron gluconate

50. SIDE EFFECTS OF PARENTERAL IRON
THERAPY
• Intra muscular- Pain, permanent skin staining.
• Intra venous – anaphylactic reaction.

51. CONCLUSION
• Iron deficiency is the most common cause of
anaemia throughout the world and is
characterized by hypochromic and microcytic red
cells
• Management involves understanding the
underlying cause and treating with oral or
parenteral iron .