Transcript What is iron-deficiency anemia

Iron deficiency anemia
Dr . YASSER AL-AHMADI
Definition of Anemia
A reduction in the concentration of
hemoglobin in the PB below the normal
for the age and sex
 WHO criteria
Adult male
Adult female
Pregnant female
< 13g/dL
< 12g/dL
< 11g/dL
Body Iron Distribution and Storage
Utilization
Duodenum
(average, 1 - 2 mg
per day)
Dietary iron
Utilization
Plasma
(TIBC)
transferrin
(3 mg)
Muscle
(myoglobin)
(300 mg)
Circulating
erythrocytes
(hemoglobin)
(1,800 mg)
Storage
iron
(Ferritin)
Liver
(1,000 mg)
Sloughed mucosal cells
Desquamation/Menstruation
Other blood loss
(average, 1 - 2 mg per day)
Iron loss
Bone
marrow
(300 mg)
Reticuloendothelial
macrophages
(600 mg)
GI Absorption of Iron
The distribution of body iron
Amount of iron
Male
in average adult
(g)
(g)
of total
Hb
2.4
1.7
65
ferritin & hemosiderin 1.0
Female
0.3
%
30
Myoglobin
0.15
0.12
3.5
Heme enzyme
0.02
0.15
0.5
Transferrin-bound
0.004
0.003
0.1
iron
Estimated daily iron requirements, Units are mg/day
Adult men
0.5-1
Postmenopausal female
0.5-1
Menstruating female
Pregnant female
Children
Female (age 12-15)
1-2
1.5-3
1.1
1.6-2.6
What is iron-deficiency anemia ?
It is the lack of iron in the blood, which is
necessary to make hemoglobin.
Causes of IDA
Increased iron requirement
Growth spurt: infants, adolescence
Menstruation
Pregnancy
Inadequate iron intake
Low iron diet
Malabsorption
Increased iron loss
GI tract
Menorrhagea
Others
Diagnosis of Anemia
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History
Physical Examination
Laboratory
Investigation
Patient History
Symptoms and its duration
Fatigue, muscle weakness, headache, vertigo,
syncope, dyspnea, palpitations, indigestion, etc
Dietary habits/Pica
Blood loss: Melena, Hematochezia, Hemorrhoid,
Menstruation(Menorrhagea)
Medications
Previous record
Family history
Physical Examination

Skin pallor
Pale conjunctiva/Jaundice
Smooth tongue/Stomatitis
Splenomegaly/Hepatomegaly

Koilonychia (Nail spooning)

Esophageal Web
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Laboratory Investigation
First Line Studies
- CBC:Hb, Hcrit, Rbc indices, Cell count, Reti count
- PB morphology examination
- Chemistry(with LDH )
Second Line Studies
- Iron/TIBC/Ferritin
- Stool occult blood(3 times)
- BM study, others
BLOOD AND
BONE MARROW SMEAR
BLOOD:
microcytosis, hipochromia, anulocytes, anisocytosis
poikilocytosis
BONE MARROW
high cellularity
mild to moderate erythroid hyperplasia (25-35%; N
16 – 18%)
polychromatic and pyknotic cytoplasm of
erythroblasts is vacuolated and irregular in outline
(micronormoblastic erythropoiesis)
absence of stainable iron
Serum iron & iron binding
capacity
Fe
TIBC
TRANSFERIN SATURATION
FERRITIN
Treatment of IDA
Correct underlying cause, if present
Iron supplementation

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Oral iron:
The best preperation is ferrous sulphate which
contains 67mg of iron in each 200mg
(anhydrous) tablet and is best given on an
empty stomach in doses spaced by at least 6
hours.if side effects occur (e.g.nausea,abd pain
,costipation or diahrea) these can be reduced
by giving iron with food or by using a
preparation of lower iron content e.g. ferrous
gluconate which contains less iron 37mg per
300mg tablet. The hb should rise at the rate of
about 2g/dl every 3 weeks.
Parentral iron
- Iron –sorbitol-citrate (jectofer) is given as
repeated i.m injections whereas ferric
hydroxide-sucrose (venofer) is administered by
slow i.v inj or infusion. There may be
hypersensitivity or anaphylactoid reactions and
parentaral iron is therefore only given when it is
considered necessary to replenish body iron
rapidly (late pregnancy or p.t on hemodialysis
and erythropoietin therapy or when oral iron is
ineffective (e.g. severe malabsorption ).the
hematological response is the same as in oral
therapy.

Q&A
When do we prescribe iron for pregnant women ?
When ferritin < 8 ng/mL
Not when ferritin > 12 ng/mL
When do we expect normalization of hemoglobin in patients with
IDA undergoing iron treatment (if no continued iron loss) ?
Usually in 4 – 6 weeks
Does intramuscular or intravenous iron restore hemoglobin level
faster than oral iron ?
No
Helicobacter pylori infection
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H. pylori infection usually acquired by oral ingestion in
childhood
Prevalence 20-50% in industrialized countries
Prevalence inversely related to socioeconomic
conditions
May be inadvertently cured by antibiotics treatment for
other reasons
Causes continuous gastric inflammation in all infected
subjects
Dr. Barry Marshall, Nobel laureate
Effects of H. pylori infection

High acid output
 Antral gastritis
 Duodenal ulcer

Low acid output
 Atrophic gastritis
 Gastric ulcer
 Gastric cancer
 MALT lymphoma
Rugae are almost completely lacking
H. pylori infection and iron
deficiency anemia

Epidemiologic studies show H. pylori (+) associated
with decreased ferritin levels
Herschko, C Best Practice Clin Hemat 2005 18:363
H. pylori infection: Mechanism of
iron deficiency
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Occult GI bleeding
Competition for dietary iron would expect more patients to be
iron deficient
Effect on gastric secretion
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High intragastric pH
Low gastric juice ascorbic acid
Possible cause of iron deficiency in
H. pylori2€
ection mediated by
achlorhydria
Annibale, B. et al. Gut 2003; 52:496
Treatment of H. pylori infection:
Effect on pH and ascorbic acid
Treatment of H. pylori
depends on presence of
atrophy
Annibale, B. et al. Gut 2003; 52:496