Iron Deficiency Anemia
Iron Deficiency Anemia
Iron Deficiency Anemia
Male 1 mg
Adolesc. 2-3 mg
Women in repr.age 2-3 mg
Pregnant 3-4 mg
Iron Metabolism
Iron absorbtion is restricted to the
needs of the body
1mg of iron is lost each day
– Sweating
– Epidermal shedding
– Menstruation and pregnancy/lactation are
other major causes of iron loss and
incresed demand in women
Iron Metabolism
Normal diet contains about 15 mg of iron/day
1/10 of ingested iron is absorbed
Gastric acid releases iron from food
Iron is absorbed in the reduced form
Ascorbate increases absorbtion (by reducing)
Phytates,tannates,antacids decrease
absorbtion by making complexes with iron
Iron Metabolism
Transport of iron
– Transferrin is the main iron carrier in
plasma
– It is produced in liver cells with increased
synthesis in iron deficiency
– Transferrin binds 1-2 ferric iron molecules
– Transferrin-iron complex is endocytosed
by Hb producing cells after linking to
receptors.
Iron Metabolism
Total iron binding capacity and iron
– Transferrin is measured by quantifying
the iron binding sites available
– This is also called “Total iron binding
capacity”
– TIBC is 1/3 saturated under normal
conditions
DIETARY IRON
Pregnancy
Lactation
Rapid growth
Decreased intake
Decreased iron in the diet
– Vegetarianism
Decreased absorbtion
– Gastric surgery
– Achlorhydria
– Sprue
– Pica
Increased iron loss
Menorrhagia
GIS hemorrhagia
•Angiodysplasia
•P.Ulcer •Diverticulosis
•Oesophagitis •Meckel diverticula
•Varices •Colitis or imf. Bovel
•Hiatal hernia disease
•Malignancy •Hemorrhoids
•NSAID use
•Parasites
Increased iron loss
Bleeding disorder
Pulmonary lesions with bleeding
Hemoglobinuria – hemosiderinuria
(chronic intravascular hemolysis)
Hemodialysis
Hematuria (chronic)
Frequent donation
– 250 mg iron /unit-blood
Clinical features
General symptoms of anemia
Fatigue may be disproportional to the degree of
anemia due to deficiency of tissue enzymes
which also need iron
Chlorosis
Glossitis
Angular stomatitis
Gastric atroph
Nail changes
– Brittle/fragility
– Koilonchia/spooning
Hair loss
Splenomegaly
Clinical features
Pica:Appetite for bizzare food/substances
– Geophagy (earth,clay)
– Pagophagia(ice)
– Amylophagia(starch)
Developmental problems
Splenomegaly
Tayanc-Prasad syndrome
(growth retardation, hypogonadism, hepatosplenomegaly, zinc and
iron deficiency, geophagia)
Immun-deficiency
Lab. Features
Hb,Htc,RBC:Low
MCV,MCH,MCHC:Low
RDW: High
Retics: Normal/Low
Plt:Normal/Low/High
WBC:Normal/Low
Smear: Hypochromia,anisocytosis,microcytosis,
poikilocytosis
Lab.Features
Serum Iron: (N: 60 – 180 μg/dL)
TIBC: (250 - 430 μg/dL)
Serum Ferritin
Microcytic anemias
– Iron deficiency anemia
– Thalassemia ,HbC,HbE etc
– Sideroblastic anemia
– Lead poisoning
– Anemia of chronic diseases (sometimes)
Important !!!!!!!
– Misdiagnosis
– Patient does not take the medicine
– Continuing blood loss
– Malabsorbtion
Change the drug
Change the route of administration
BY DR PP GEVAO
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Thalassemia
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Thalassemia
• Diverse group of disorders which manifest
as anemia of varying degrees.
• Result of defective production of globin
portion of hemoglobin molecule.
• Distribution is worldwide.
• May be either homozygous defect or
heterozygous defect.
• Defect results from abnormal rate of
synthesis in one of the globin chains.
• It is an autosomal recessive syndrome
Thalassemia
• Results in overall decrease in amount of
hemoglobin produced and may induce
hemolysis.
• Two major types of thalassemia:
– Alpha (α) - Caused by defect in rate of synthesis
of alpha chains.
– Beta (β) - Caused by defect in rate of synthesis in
beta chains.
• May contribute protection against malaria.
Genetics of Thalassemia
γ4 β4
Hemoglobin H Disease
• Live normal life; however, infections,
pregnancy, exposure to oxidative drugs may
trigger hemolytic crisis.
• RBCs are microcytic, hypochromic with marked
poikilocytosis. Numerous target cells.
• Hb H vulnerable to oxidation. Gradually
precipitate in vivo to form Heinz-like bodies of
denatured hemoglobin. Cells been described
has having "golf ball" appearance, especially
when stained with brilliant cresyl blue.
Bart’s Hydrops Fetalis Syndrome
• Most severe form. Incompatible with life. Have no
functioning alpha chain genes (--/--).
• Baby born with hydrops fetalis, which is edema and ascites
caused by accumulation serous fluid in fetal tissues as result
of severe anemia. Also see hepatosplenomegaly and
cardiomegaly.
• Predominant hemoglobin is Hemoglobin Bart, along with
Hemoglobin Portland and traces of Hemoglobin H.
• Hemoglobin Bart's has high oxygen affinity so cannot carry
oxygen to tissues. Fetus dies in utero or shortly after birth. At
birth, see severe hypochromic, microcytic anemia with
numerous NRBCs.
• Pregnancies dangerous to mother. Increased risk of toxemia
and severe postpartum hemorrhage.
Comparison of Alpha Thalassemias
Genotype Hb A Hb Bart Hb H
Normal 97-98% 0 0
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Differential Diagnosis of Microcytic,
Hypochromic Anemias