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Etiology:
Normal
Iron Physiology
-
·
Total body Fe+
≈ 2 – 5 g in average adult.
-
·
Most is present in
meat & vegetables.
-
·
Transferrin obtains
Fe+ mainly from RE (MØ).
Only a small proportion of plasma Fe+ comes
from dietary Fe+ absorbed through duodenum
& jejunum.
·
N.B.
Ferritin:
·
N.B.
Hemosiderin:
N.B.
Ceruloplasmin (Cu+2 –containing enzyme) catalyzes
oxidation into Fe+3 for binding to plasma transferrin.
 |
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Duodenum |
v
Distribution
of body Fe+
consists of:
Hb,
Ferritin & Hemosiderin (storage), Mb, Heme enzymes (catalase,
cytochromes, peroxidases), Transferrin.
v
Factors
↑
Fe+
absorption:
1.
Fe+2 form.
2.
Inorganic Fe+.
3.
Fe+ def.
4.
↑ Erythropoietin.
5.
Acids (HCl, Vit. C)
6.
Pregnancy.
7.
1º Hemochromatosis.
v
Factors
↓
Fe+ absorption:
5.
Alkali (antacids, pancreatic secretions).
6.
Infection.
7.
Tea.
8.
Desferrioxamine (Fe+ chelating agent).
N.B.
IRON
DEFICIENCY
·
The development of Fe+
deficiency anemia:
v
Causes:
Table
1.
Causes of
iron deficiency. Note that the commonest cause is hookworm infection worldwide.
o
Uterine.
o
GI:
e.g. hookworms, esophageal varices, hiatus hernia, PU, partial
gastrectomy, NSAIDs, Ca of stomach, cecum, colon, rectum,
angiodysplasia, piles, diverticulosis, colitis.
↑ demands:
o
Prematurity.
o
Adolescent growth.
o
Child-bearing.
Malabsorption:
gastrectomy, celiac dis.
Poor diet:
Vegans, elderly.
v
Clinical
Features:
o
Angular
stomatitis.
o
Koilonychia.
o
Dysphagia
due to pharyngeal webs (Plummer-Vinson syndrome).
v
Lab
Diagnosis:
1.
Blood
film:
o
Hypochromic microcytic
RBCs.
o
Target cells +
pencil-shaped poikilocytes.
o
Anisocytosis (↑
RDW).
N.B.
Dimorphic film:
Ø
Macrocytic &
microcytic hypochromic cells.
Ø
Seen also in patients
with Fe+ def. who
have received recent Fe+ therapy / by transfusion.
Ø
Indices may be normal.
2. CBC :
 |
o
Hb, MCV, MCH, MCHC.
o
Retics. |
|
|
o
S-transferrin.
o
S-Fe+
& TIBC
à
% Saturation ¯
o
BM-Fe+
: absent !!
|
Fig.
The serum iron.
Note that ↑ S-ferritin à
Fe+ overload / excess release of ferritin from damaged
tissue (e.g. acute hepatitis).
ANEMIA
OF CHRONIC DISEASES
q
Probably 2nd commonest form of anemia.
v
Causes:
1.
Chronic inflammatory Diseases:
Ø
Infection :
Pulm. abscess, TB, OM, Pneumonia.
Ø
Non-infectious :
RA, SLE, Sarcoidosis, Crohn’s, Hepatitis.
2.
Malignancies:
Ø
Carcinoma,
lymphoma, sarcoma.
v
Pathophysiology:
q
Exactly unknown, but 3 mechanisms are involved:
|
RE
(MØ) in BM
|
|
Erythroblasts
|
|
↓
Fe+ in erythroblasts.
|
↓ RBCs
lifespan.
3.
↓ Production of erythropoietin.
q
Severity of anemia reflects severity & duration of
disease.
q
Anemia is only corrected by successful treatment of
underlying disease & doesn’t respond to Fe+
therapy.
v
Lab
Diagnosis:
q
↓ Hb,
↓ Hct,
↓ S-Fe+,
↓ TIBC.
q
% Saturation (S-Fe+/TIBC):
N
q
BM-Fe+
N / ↑
q
Ferritin
N / ↑
(infection / malignancy à
↑ Ferritin)
SIDEROBLASTIC
ANEMIA
v
Defect
in heme synthesis.
v
Classification:
Ø
X-linked.
Ø
Due to defect in δALA synthetase / heme synthetase.
o
Acquired:
Ø
1º :
Myelodysplasia FAB type 2 (refractory anemia with ring
sideroblasts)
Ø
2º :
§
Malignancies of BM: AML, Other types of Myelodysplasia.
§
Anti-Tb (INH), alcohol, lead.
§
Megaloblastic anemia.
v
Lab
Diagnosis:
BM à
Fe+ stain.
(Ring
sideroblasts) = Fe+
granules around nucleus of erythroblasts.
written
by:
Khalid Bin Yaroof. FMHS, UAE University.
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