Hematinics – Types (Pharmacology)


  • An agent that tends to stimulate blood cell formation or to increase the hemoglobin in the blood.
  • Or used for the prevention and treatment of anemia.


  • Formed in the red bone marrow.
  • It is a conjugated protein, consisting of an iron-containing pigment combined with histone (protein) is known as Globin.
  • The iron-containing protein is a porphyrin consisting of 4 pyrrole rings.
  • This porphyrin is designated as Heam.
  • Folic acid and vitamin B12 are capable of increasing the rate of Heam synthesis in the red cells.


  • A condition in which the blood is deficient in the RBC (erythrocytes), in hemoglobin.
  • Or deficiency in quality or the quantity of blood.
  • Erythrocytes are mainly responsible for delivering oxygen to the tissues, less RBC means less oxygen to tissues.

4 types:

  • Microcytic anemia: Deficiency of iron (Fe).
  • Macrocytic anemia: Deficiency of folic acid and B12.
  • Hemolytic anemia: Abnormal breakdown of RBCs.
  • Aplastic anemia: The body stops producing new blood cells.


  • IRON.
  • FOLIC ACID (pteroylglutamic acid).
  • VITAMIN B12 (cyanocobalamin).


  • The human body contains about 3.5 gm of iron of which about 2/3 is contained in the blood.
  • 5 – 10% of ingested iron is absorbed.
  • Once ingested the acid in the stomach:

1. Aids in ionization of iron

2. Splits chelated food iron from the chelator

3. Maintains iron insoluble form 4. Allows iron to remain in the absorbable form Fe3+.

Mechanism of Iron Absorption:

  • Iron absorption occurs all over the intestine.
  • In the stomach, which contains HCL and reducing agent, convert the ferric to ferrous.
  • Two separate iron transporters in the intestinal mucosal cells function to affect iron absorption.
  • At the luminal membrane, the divalent metal transporter 1 (DMT) carries ferrous iron into the mucosal cell.
  • The ferroportin is bound with ferrous iron and pass through mucosal cell directly into the bloodstream.
MoA of Iron Absorption - Hematinics
Fig.1: MoA of Iron Absorption

Transport, Utilization, Storage, and Excretion:

  • As such, on entering plasma it is immediately converted to the ferric form and complexed with glycoprotein transferrin (Tf).
  • Iron is transported into erythropoietic and other cells through the attachment of transferrin receptor (Tf Rs).
  • The complex is engulfed by receptor-mediated endocytosis.
  • Iron dissociates from the complex at the acidic pH of the intracellular vesicles.
  • The released iron is utilized for hemoglobin synthesis or other purposes.
  • Tf and Tf R are returned to the cell surface to carry fresh loads.


  • Reticuloendothelial cells
  • Spleen
  • Bone marrow
  • Hepatocytes and myocytes.

Therapeutic uses of Iron:

  • Iron Deficient Anemia
  • Pregnancy
  • Premature Babies
  • Blood loss
  • Hookworn infestation
  • Malabsorption Syndrome
  • GI Bleeding due to Ulcers, Aspirin, Excess consumption of coffee.

Iron Preparations:

Oral Iron:
  • Ferrous Sulfate (Feosol) – 300 mg bid.
  • Side Effects are extremely mild:
  1. Nausea, upper abdominal pain, constipation, or diarrhea.
  2. The cheapest form of Iron and one of the most widely used.
  • Iron Dextran (Imferon) – IM or IV
  • Indicated for patients who cannot tolerate or absorb oral iron or where oral iron is insufficient to treat the condition ie. Malabsorption syndrome, prolonged salicylate therapy, dialysis patients.


  • A source of food – yeast, egg yolk, liver, and leafy vegetables.
  • Folic Acid (F.A.) is absorbed in the small intestines.
  • F.A. is converted to tetrahydrofolate by dihydrofolate reductase.
  • Folic Acid deficiency (F.A. Deficiency) is also called Will’s Disease.
  • Deficiency may produce megaloblastic anemia; neural tube defects in the fetus.

Therapeutic Uses of Folic Acid:

  1. Megaloblastic Anemia due to inadequate dietary intake of folic acid:
  • Can be due to chronic alcoholism, pregnancy, infancy, impaired utilization: uremia, cancer, or hepatic disease.

2. To alleviate anemia that is associated with dihydrofolate reductase inhibitors:

  • i.e. Methotrexate (Cancer chemotherapy), Pyrimethamine (Antimalarial)
  • Administration of citrovorum factor (methylated folic acid) alleviates anemia.

3. Ingestion of drugs that interfere with intestinal absorption and storage of folic acid:

  • Mechanism: Inhibition of the conjugases that break off folic acid from its food chelators.
  • Example: Phenytoin, Progestin/estrogens (oral contraceptives)

4. Malabsorption: Sprue, Celiac disease, partial gastrectomy.

5. Rheumatoid arthritis: Increased folic acid demand or utilization.


  • Synthetic folic acid daily 10-30mg orally is given.


  • Non-toxic to man.



  • In food, especially in the liver and kidneys. GI Microorganism synthesis, Vitamin Supplements (Cyanocobalamin).
  • Necessary for normal DNA synthesis.

Absorption of B12:

1. Intrinsic Factor (low dose): A protein made by stomach parietal cells that bind to B12 and delivers it from the ileum via a calcium-mediated event.

2. Mass Action (High dose): 1000 mg/day, absorbed via passive diffusion.

Distribution of B12:

Vitamin B12 is distributed to various cells bound to a plasma glycoprotein, Transcobalamin II.

Storage of B12:

  • Excess vitamin B12 (up to 300-500 microgram) is stored in the liver.

Therapeutic Uses of B12:

  • Daily Requirements – 0.6 – 1.0mh/day; T1/2 ~ 1 year.
  • Pernicious Anemia.
  • Impaired GI absorption of B12.
  • Gastrectomy.
  • Corrosive Injury of GI mucosa.
  • Fish tapeworm: worm siphons off B12.
  • Placebo abuse with B12, especially in elderly patients.
  • Malabsorption syndrome.
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