Dr. Rajasekara. S Associate professor, Dept. of Pharmacology, Malik deenar college of pharmacy, Kerala

1. DUGS EFFECTIVE IN DIFFERENT
TYPES OF ANAEMIAAND ITS
PHARMACOTHERAPY
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2. • Anemia is a decrease in the number of red blood
cells (RBCs), a decrease in the amount of
hemoglobin in RBCs, or both
• When there is an insufficient amount of
hemoglobin to deliver oxygen to the tissues,
anemia exists.
• There are various types and causes of anemia.
• For example, anemia can be the result of blood
loss, excessive destruction of RBCs, inadequate
production of RBCs, and lack of various nutrients

3. TYPES OF ANAEMIA:
Iron defiency anaemia
Aplastic anaemia
Megaloblastic anaemia
Haemolytic anaemia
Sickle cell anaemia
Pernicious anaemia
Sideroblastic anaemia
Normocytic normochromic anaemia

4. Iron Deficiency Anaemia
• Iron deficiency is the most common cause of chronic
anemia
• Iron is a component of hemoglobin, which is in RBCs.
• It is the iron in the hemoglobin of RBCs that picks up
oxygen from the lungs and carries it to all body tissues
• When the body does not have enough iron to supply the
body’s needs, the resulting condition is iron deficiency
anemia.

5. oral iron
• A) Ferrous sulfate - 325mg - 65mg elemental
iron
• B )Ferrous gluconate - 320mg -37mg
elemental iron
• C) Ferrous fumarate - 325mg - 106mg
elemental iron
Parenteral iron: iron dextran 50mg elemental
iron/ml

6. Treatment of iron deficiency anemia
• Iron salts, such as ferrous sulfate or ferrous
gluconate, are used in the treatment of iron
deficiency anemia,
• Iron dextran is a parenteral iron that is also used
for the treatment of iron deficiency anemia.
• It is primarily used when the patient cannot take
oral drugs or when the patient experiences
gastrointestinal intolerance to oral iron
administration.

7. Pharmacokinetics
• Iron is normally absorbed in the duodenum and
proximal jejunum
• Iron is transported in the plasma bound to
transferrin, a -globulin that specifically binds
ferric iron.
• Iron is stored, primarily as ferritin, in intestinal
mucosal cells and in macrophages in the liver,
spleen, and bone.
• There is no mechanism for excretion of iron.
Small amounts are lost by exfoliation of intestinal
mucosal cells into the stool, and trace amounts
are excreted in bile, urine, and sweat.

8. ADVERSE REACTIONS
• Iron salts occasionally cause gastrointestinal
irritation, nausea, vomiting, constipation, diarrhea,
headache, backache, and allergic reactions.
• The stools usually appear darker (black).
• Iron dextran is given by the parenteral route.
Hypersensitivity reactions, including fatal
anaphylactic reactions, have been reported with
the use of this form of iron.

9. • Additional adverse reactions include soreness,
inflammation, and sterile abscesses at the
intramuscular (IM) injection site.
• Intravenous (IV) administration may result in
phlebitis at the injection site.
• When iron is administered via the IM route, a
brownish discoloration of the skin may occur.
Patients with rheumatoid arthritis may
experience an acute joint pain, and swelling may
occur when iron dextran is administered.

10. CONTRAINDICATIONS AND INTERACTIONS
• Drugs used to treat anemia are contraindicated in
patients with known hypersensitivity to the drug
• Iron compounds are contraindicated in patients with
any anemia except iron deficiency anemia
• Oral iron preparations are Pregnancy Category B
drugs; iron dextran is a Pregnancy Category C drug.
The iron preparations are used cautiously during
pregnancy and lactation.
• Iron dextran is used cautiously in patients with
cardiovascular disease, a history of asthma or
allergies, and rheumatoid arthritis (may exacerbate
joint pain).

11. • The absorption of oral iron is decreased when the
agent is administered with antacids, tetracyclines,
penicillamine, and the fluoroquinolones.
• When administered orally, iron deceases the
absorption of levodopa.
• Ascorbic acid increases the absorption of oral
iron.
• Iron dextran administered concurrently with
chloramphenicol increases serum iron levels.

12. Megaloblastic anemia
• Folic acid is required for the manufacture of
RBCs in the bone marrow.
• Folic acid is found in leafy green vegetables,
fish, meat, poultry, and whole grains.
• A deficiency of folic acid results in megaloblastic
anemia. Megaloblastic anemia is characterized by
the presence of large, abnormal, immature
erythrocytes circulating in the blood.

13. ACTION AND USES
• Folic acid is used in the treatment of megaloblastic
anemias that are caused by a deficiency of folic
acid.
• Leucovorin is a derivative (and active reduced
form) of folic acid. The oral and parenteral forms of
this drug are used in the treatment of megaloblastic
anemia.
• Leucovorin may also be used to diminish the
hematologic effects of (intentional) massive doses
of methotrexate, a drug used in the treatment of
certain types of cancer. Leucovorin “rescues”
normal cells from the destruction caused by
methotrexate and allows them to survive.

14. Pharmacokinetics
• which is usually absorbed, depending on
metabolic requirements (pregnant women may
absorb as much as 300–400g of folic acid daily).
• The richest sources are yeast, liver, kidney, and
green vegetables.
• Normally, 5–20 mg of folates are stored in the
liver and other tissues.
• Folates are excreted in the urine and stool and are
also destroyed by catabolism,

15. ADVERSE REACTIONS
• Few adverse reactions are associated with the
administration of folic acid and leucovorin.
• Rarely, parenteral administration may result in
allergic hypersensitivity.

16. CONTRAINDICATIONS AND
INTERACTIONS
• Folic acid and leucovorin are contraindicated for
the treatment of pernicious anemia
• Use of aminosalicylic with folic acid may
decrease serum folate levels.
• Folic acid utilization is decreased when folate is
administered with methotrexate.
• Signs of folic acid deficiency may occur when
sulfasalazine is administered concurrently.
• An increase in seizure activity may occur when
folic acid is administered with the hydantoins.

17. Aplastic anemia
• Aplastic anaemia develops as a result of bone marrow
damage.
• This causes a deficiency of all three blood cell types
(pancytopenia): red blood cells (anemia), white blood cells
(leukopenia), and platelets (thrombocytopenia).
• The damage may be present at birth or occur after exposure
to radiation, chemotherapy, toxic chemicals, some drugs or
infection.

18. Diagnosis :
• Blood tests. Normally, red blood cell, white blood
cell and platelet levels stay within a certain range.
• Bone marrow biopsy. To confirm a diagnosis,
you'll need to undergo a bone marrow biopsy. In
this procedure, a doctor uses a needle to remove a
small sample of bone marrow from a large bone in
your body, such as your hipbone. The bone
marrow sample is examined under a microscope
to rule out other blood-related diseases.
• In aplastic anemia, bone marrow contains fewer
blood cells than normal.

19. Treatment
Blood transfusions
• Red blood cells. Transfusions of red blood cells
raise red blood cell counts. This helps relieve anemia
and fatigue.
• Platelets. Transfusions of platelets help prevent
excessive bleeding.
Stem cell transplant
• A stem cell transplant to rebuild the bone marrow
with stem cells from a donor may offer the only
successful treatment option for people with severe
aplastic anemia. A stem cell transplant, which is also
called a bone marrow transplant

20. Immunosuppressants
• Drugs such as cyclosporine and anti-thymocyte
globulin are examples. These drugs suppress the
activity of immune cells that are damaging our bone
marrow. Cyclosporine and anti-thymocyte globulin
are often used in combination.
• Corticosteroids, such as methylprednisolone are
often given at the same time as these drugs.
Bone marrow stimulants
• Certain drugs — including colony-stimulating
factors, such as sargramostim, filgrastim,
pegfilgrastim and epoetin alfa — may help stimulate
the bone marrow to produce new blood cells.

21. Pharmacokinetics
• The absorption of cyclosporine from the
gastrointestinal tract is incomplete and variable.
• metabolized by the cytochrome P450 3A enzyme
system in the liver.
• Elimination is primarily biliary with only 6% of
the dose (parent drug and metabolites) excreted in
the urine. Only 0.1% of the dose is excreted in the
urine as unchanged drug.

22. ADVERSE REACTIONS
• decreased appetite
• dizziness
• drowsiness
• fever
• headache
• muscle spasms (tetany) or twitching
• nausea and vomiting
• nervousness
• painful or difficult urination
• white spots on the lips or in the mouth

23. Drug Interactions
• Aceclofenac may increase the nephrotoxic
activities of Cyclosporine.
• The metabolism of Cyclosporine can be
decreased when combined with 2-Hydroxy-1,4-
Naphthoquinone.
• The serum concentration of Cyclosporine can be
increased when it is combined with 1,10-
Phenanthroline.