Iron Deficiency Anemia 21-Oct-2014

 Most common cause of anemia in the world

 Frequent loss may lead to hemorrhage.
 Average daily diet contains 15-20 mg iron & only 10% is absorbed
 Absorption may be increased upto 20-30 % in iron deficiency and
pregnancy.
 2/3 of iron is present as haemoglobin (2.5 -3 g in normal adult)
 Iron stored in reticuloendothelial cells,hepatocytes & skeletal muscles
cells – 500-1500mg.
 Normal Serum Iron level - 13-32 μmol/L
 There is a diurnal rhythm with higher levels in the morning.
 Each day 0.5-1.0 mg of iron is lost in the faeces, urine and sweat.

Iron transport in the plasma.

 Bound to transferrin, a β-globulin that is synthesized in the liver.

 Each transferrin molecule binds two atoms of ferric iron and is normally
one-third saturated.

Causes of Iron Deficiency :

 Poor Intake of iron food

 Malabsorption (due to use of antacids , celiac disease, gastrectomy,
 High intake of inhibitors of iron absorption (PPIs)
 Hook worm infestations
 schistosomiasis
 Blood loss
 ↑ demands such as pregnancy & rapid growth, such as infancy and
puberty.
 Low iron stores

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 Clinical Features

Symptoms:

 Fatigue
 Dizziness
 Palpitations
 Chest Pain
 Intermittent claudication

Signs:

 Pallor
 Smooth tongue(Chelosis)
 Koilonychias
 Splenomegaly
 Brittle hair
 Plummer-Vinson Syndrome: dysphagia and glossitis associated with iron
deficiency anemia

Investigations
BLOOD COUNT AND FILM

 A characteristic blood film shows ,red cells are

 Microcytic (MCV < 80 fL) and hypochromic (MCH < 27 pg).
 There is poikilocytosis (variation in shape) and anisocytosis (variation in
size).

Serum Ferritin:

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  The level of serum ferritin reflects the amount of stored iron.
 Normal values for serum ferritin are
30-300 μg/L (11.6-144 nmol/L) in males
15-200 μg/L (5.8-96 nmol/L) in females.
 In simple iron deficiency, a low serum ferritin confirms the diagnosis.

Serum Soluble Transferrin Receptors & TIBC:

 The number of transferrin receptors increases in iron deficiency.

 Serum iron falls & total iron binding capacity (TIBC) rises.
 Helpful to distinguish between iron deficiency and anemia of chronic
disease, and may avoid the need for bone marrow examination even in
complex cases.
 As plasma iron increases in liver disease & haemolysis.

Bone Marrow:

 Erythroid hyperplasia with ragged normoblasts is seen in the marrow in

iron deficiency.
 Staining using Perls' reaction (acid ferrocyanide) does not show the
characteristic Prussian-blue granules of stainable iron in the bone
marrow fragments or in the erythroblasts.
 

Differential Diagnosis:
 The presence of anemia with microcytosis and hypochromia does not
necessarily indicate iron deficiency.
 Most common other causes are
 Thalassemia
 Sideroblastic anemia
 Anemia of chronic disease
 In these disorders the iron stores are normal or increased.

Treatment

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  Find & treat the underlying cause
 Give iron to correct anemia.
 Replace iron stores.
 Response to iron therapy can be monitored using the reticulocytes count
& Hb level.

Oral Iron:

 Oral iron is all that is required in most cases.

 Best preparation is Ferrous Sulphate 200 mg three times dail which is
absorbed best when the patient is fasting.
 If the patient has side-effects such as nausea, diarrhea or
constipation take the tablets with food or reduce the dose or use a
preparation with less iron such as Ferrous Gluconate
 The use of expensive iron compounds, particularly the slow-release
ones which release iron beyond its main sites of absorption, is
unnecessary.
 Blood transfusion if heart failure is eminent
Parental Iron:

 Parenteral iron is required by occasional patients:

 Those who have general intolerance of oral preparations even at low
dose.
 Those with severe malabsorption.
 Those who have chronic gastrointestinal diseases such as ulcerative
colitis or Crohn's disease.

Prevention of IDA

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Dietary modification:
 Eat more fruits and vegetable
 No coffee or tea with meals
 Programs should be targeted to at risk groups
 Reduce phytic content of cereals and legumes by fermentation.

 Short term approach:

Supplementation with iron tablets.

 Long-term approach:
Food fortification with iron either for the whole population (blanket
fortification) or for specific target groups like infants.

_________________ END __________________

Megaloblastic Anemia

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This results from a deficiency of vitamin B12or folic acid, or from disturbances
in folic acid metabolism. Results in delayed nuclear development, causing the
larger cells. Deficiency of either vitamin B12or folate will therefore produce
high plasma levels of homocysteine and impaired DNA synthesis resulting in
delayed or stopped cell division in bone marrow.

It is characterized by large erythrocytes ( MCV> 100) – Macrocytic anemia.

Vitamin B12
The average daily diet contains 5–30 μg of vitamin B12, mainly in meat, fish,
eggs, poultry and milk (and other dairy products ) —well in excess of the 1
μg daily requirement.

Deficiency of vitamin B12:

1- Inadequate dietary intake

2- Malabsorption.
3- Gastric factors
 Release of vitamin B12 from the food requires normal gastric acid
and enzyme secretion, and this is impaired by hypochlorhydria in
elderly patients or following gastric surgery.
 Total gastrectomy invariably results in vitamin B12 deficiency
within 5 years, often combined with iron deficiency.

Pernicious Anemia:

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It is the megaloblastic anemia due to Vit B12 deficiency as a result of failure of
secretion of intrinsic factor by stomach due to atrophy of gastric mucosa
(autoimmune disorder). In the absence of intrinsic factor, less than 1% of
dietary vitamin B12is absorbed.it is commonest cause of vit. B12 deficiency.

Folic Acid

Foods rich in folic acids are liver, kidney, spinach, cabbage, potato, banana.

Investigations:
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  Granulocytes and Thrombocytes are affected as well.
 Granulocytes are hypersegmented
 Megakaryoctyes are abnormal resulting in thrombocytopenia

Schilling test:

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  Establishes the cause of vitamin B12 deficiency
 Test performed in two parts
 If parts one & two abnormal: Pernicious anemia
 If part one only abnormal: malabsorption


Treatment
B12 deficiency

 Vitamin therapy
 Intramuscular or subcutaneous injections for pernicious anemia to
bypass absorption through the gut.
 Vitamin B12 deficiency is treated with hydroxycobalamin
 1mg I.M. in five doses 2 or 3 days apart, followed by maintenance
therapy of 1mg every 3 months for life.

Folate deficiency

 Vitamin therapy
 Oral folic acid 5 mg daily for 3 weeks will treat acute deficiency and 5 mg
once weekly is adequate maintenance therapy.

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Anemia of chronic disease (ACD)

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ACD is a common type of anemia that occurs in patients with infectious,
inflammatory, or neoplastic diseases that persist for more than 1 or 2 months.

ACD is more common that any anemia syndrome other than blood loss with
consequent iron deficiency. This is a common type of anaemia, particularly in
hospital populations.

 There is decreased release of iron from bone marrow to developing

erythroblasts.
 Decreased response to erythropoietin.
 Decreased RBCs survival.

Disorders Associated with the Anemia of Chronic Disease ACD

 Chronic Infections.
 Pulmonary infections: Tuberculosis, pneumonia
 Subacute bacterial endocarditis
 Chronic urinary tract infections
 Osteomyelitis.

 Chronic, non-infectious inflammations:

 Rheumatoid arthritis
 Systemic lupus erythematous

 Malignant diseases:
 Cancer
 Hodgkin’s disease and Non-Hodgkin’s Lymphomas.

Anemia of chronic disease (ACD) – pathogenesis:

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  Shortened red cell life span, moderately 20-30% (from 120 to 60-90
days).
 Relative bone marrow (erythropoiesis) failure.
 ABNORMAL IRON METABOLISM
 Impaired release of iron from macrophages to circulating
transferrin (impaired reutilization of iron).
 The iron remains trapped inside the cells in the form of ferritin, levels of
which are therefore normal or high.

Treatment:

 Treat the underlying cause.

 Transfusion
 A trial of oral iron can be given in difficult situations.

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Aplastic Anemia
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Aplastic Anemia is defined as peripheral blood pancytopenia (↓ RBC, WBC,
platelets) with aplasia (inability to produce blood cells) of the bone marrow.

It is due to reduction in the number of the pluripotenial stem cells. Failure one
cell line may occur more than others.

Causes of Aplastic Anemia:

 Inherited: Fanconi’s Anemia

 Acquired: Idiopathic
 Drug : Acetazolamide, Carbamazepine, Gold, Phenylbutazone,
azathioprine
 Infections: HIV, viral hepatitis, TB
 Chemical: benzene
 Radiation exposure
 Viral illness
 Pregnancy

Pathogenesis:

 Immune mechanism responsible for most of the cases of Idiopathic

acquired aplastic anemia.
 Activated Cytotoxic T cells in Blood & Bone marrow →Bone marrow
failure.

Clinical Features:

 Anemia – due to low RBC

 Infection – due to low WBC
 Bleeding –due to low platelets
 Fatigue , pallor , dyspnea , due to anemia
 Petechiae, ecchymosis – bleeding disorder due to low platelet count.

Treatment

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  Treatment of underlying cause –if possible
 Supportive care:
 Packed cell volume and platelet transfusion for bleeding
 Antibiotics for infection.
 Blood transfusion.
 Bone Marrow Transplant:
 There is treatment of choice for patients under 40 years who have HLA
identical donor.

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