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Iron deficiency anaemia

Iron deficiency anaemia


IRON DEFICIENCY ANEMIA

  • Hypochromic anemia can be due to iron deficiency.
  • Commonest nutritional deficiency disorder throughout the world is iron deficiency.
  • Storage form of iron is serum ferritin (Fe+3) in liver, spleen, bone marrow.

Iron Metabolism-

  • Heme iron is better absorbed than non heme iron.
  • Heme iron enters mucosal cells and non heme iron is first reduced to ferrous iron and then absorbed in duodenum.
  • Then, it is transported inside enterocytes via apical transport called DMT1 (divalent metal transporter 1).
  • Absorbed iron transported to basememnt membrane which requires ferroprotein & Hephaestin for conversion of ferrous to ferric form.
  • Iron hemostasis is regulated by Hepacidin which degrades to ferroprotein & iron absorption.
  • This iron taken up by transferring will be delivered to bone marrow & hepatocytes.
  • Finally ferric iron will be utilized for maturation of erythroid precursors.
  • DMT1 also facilitates uptake of cadium & lead.

Iron excretion-

  • Amount of iron lost per day- 0.5 – 1 mg.

Pathogenesis-

  • Increase blood loss
  • Increase requirements
  • Inadequate dietry intake
  • Decreased intestinal absorption

Factors affecting iron absorption- 

Clinical Features-

  • Anaemia
  • Weakness, fatigue, pallor of skin
  • Menorrhagia
  • Koilonychia
  • Atrophic glossitis
  • Angular stomatitis
  • Plummer Vinson syndrome

Lab findings-

  • Anaemia- iron level indicated by reticulocytosis
  • Haemoglobin decreased
  • RBC- hypochromic & microcytic
  • Anisocytosis & poikilocytosis
  • Reticulocytes count is normal.
  • MCV, MCH, MCHC-  reduced.
  • WBC count is normal.
  • Platelets count normal.

Bone marrow findings-

  1. Marrow cellularity increased
  2. Erythropoiesis- micronormoblasts
  3. Iron staining on bone marrow aspirate shows decrease iron stores (Prussian blue reaction)

Biochemical findings-

  1. Serum level decrease
  2. TIBC increase
  3. Serum ferrritin decrease
  4. Red cell protoporphyrin decrease
  5. Serum transferring receptors protein increased. (STFR to log of ferritin) 

Treatment-

  • Correction of iron deficiency.

Oral therapy-

  1. Oral iron salts (0-3 months)- 100- 150 mg
  2. Parentral therapy- Iron dextran may be given IM or IV.

Exam Important

  • Hypochromic anemia can be due to iron deficiency.
  • Commonest nutritional deficiency disorder throughout the world is iron deficiency.
  • Storage form of iron is serum ferritin (Fe+3) in liver, spleen, bone marrow.

IRON METABOLISM

  • Heme iron enters mucosal cells and non heme iron is first reduced to ferrous iron and then absorbed in duodenum.
  • Then, it is transported inside enterocytes via apical transport called DMT1 (divalent metal transporter 1).
  • Absorbed iron transported to basememnt membrane which requires ferroprotein & Hephaestin for conversion of ferrous to ferric form.
  • Finally ferric iron will be utilized for maturation of erythroid precursors.
  • DMT1 also facilitates uptake of cadium & lead.

Iron excretion-

  • Amount of iron lost per day- 0.5 – 1 mg.

Clinical Features-

  • Weakness, fatigue, pallor of skin
  • Plummer Vinson syndrome
  • Plummer Vinson syndrome

Lab findings-

  • Anaemia- iron level indicated by reticulocytosis
  • Haemoglobin decreased
  • RBC- hypochromic & microcytic
  • Anisocytosis & poikilocytosis
  • Reticulocytes count is normal.
  • MCV, MCH, MCHC-  reduced.
  • WBC count is normal.
  • Platelets count normal.

Bone marrow findings-

  1. Marrow cellularity increased
  2. Erythropoiesis- micronormoblasts
  3. Iron staining on bone marrow aspirate shows decrease iron stores (Prussian blue reaction)

Biochemical findings-

  1. Serum level decrease
  2. TIBC increase
  3. Serum ferrritin decrease
  4. Red cell protoporphyrin decrease
  5. Serum transferring receptors protein increased. (STFR to log of ferritin)

TREATMENT 

  1. Oral iron salts (0-3 months)- 100- 150 mg
  2. Parentral therapy- Iron dextran may be given IM or IV.
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