Drugs for iron def anemia

Drugs for iron deficiency anemia

1. DR.SARITHA,
ASST PROFESSOR,
DEPT OF PHARMACOLOGY

2. • Decrease in oxygen carrying capacity of blood is called
anaemia.

• Oxygen carrying capacity of blood is determined by
hemoglobin content of cells.
• Reduction in blood hemoglobin levels &
no of circulating erythrocytes are characteristic
features of anaemia.

3. The haematopoietic machinery – present in the bone
marrow.
It is primarily involved in the formation of cellular
components of the blood – erythrocytes, leucocytes &
thrombocytes.
 For proper functioning – needs
Exogenous nutrients – Iron, vitB
12
& folic acid called
haematinics.
Endogenously derived growth factors – (G-CSF), (GM-
CSF), Erythropoietin, thrombopoietins, IL-1,3,5,6,7,11
etc.
Reduction in the supplies of any of these nutrients –
results in deficiency of normal blood cells.

4. ANAEMIAS due to dietary deficiency or
malabsorption of factors essential for normal blood
formation .
e.g: iron ,folic acid , vitamin B12,vit C ,pyridoxine
DUE TO BLOOD LOSS - menorrhagia ,GI loss,
hookworm infestation.
DUE TO EXCESSIVE BLOOD DESTRUCTION
thalassemia, sickle cell ,auto immune hemolytic
anaemia.

5. DUE TO APLASIA OR HYPOPLASIA OF BONE
MARROW
- Anti cancer drugs and chloramphenicol

DUE TO DEFICIENCIES OF ERYTHROPOIETIN
- Chronic renal disease
UNCERTAIN ORIGIN
- Infection, rheumatoid arthritis ,malignant disease

6. These are the substances required in the
formation of blood, and are used for the
treatment of anemias.
- Iron, vitB
12
& folic acid

7.  Most common disorder in clinical practice.
Charectarized by a decrease in the O2 carrying
capacity of the blood due to reduced
concentration of Hb or RBCS

8.  IRON DEF ANAEMIA CHARACTERISED BY-
MICROCYTOSIS (presence of small erythrocytes).
HYPO CHROMIA ( poorly filled with haemoglobin).
POIKILOCYTOSIS (bizzare shaped cells).
ANISOCYTIOSIS (different shapes).
Iron def has adverse effects on brain function,
mental performance & ,behavioral abnormalities.

10. Iron(Fe) is the essential body constituent .
Total body iron in an adult –
2.5 – 5 g (average 3.5g).
It is more in men - (50mg/kg)
Than in women (38mg/kg)
It is distributed as follows :
Hemoglobin (Hb) – 66%
Iron stores ferritin and Haemosiderin – 25%
Myoglobin ( in muscles) – 3%
Parenchymal iron (in enzymes etc) – 6%

11. Loss of 100ml of blood (containing 15g Hb) means loss of
50mg elemental iron.
To raise Hb level of blood by 1g/dl about 200mg of iron is
needed.
Daily requirement of iron
Adult male – 0.5 – 1 mg (13mg/kg)
Adult female – 1 – 2 mg (21mg/kg)
(Menstruating)
Infants – 60mg/kg
Children – 25 mg/kg
Pregnancy – 3.5 mg (80mg/kg)
(Last 2 trimesters)

12. DIETARY SOURCES OF IRON
Rich → liver, egg yolk, oyster, drybeans, dry fruits, wheat germ,
yeast.
Medium → meat, chicken, fish, spinach, banana, apple.
Poor → milk and its products, root vegetables.

13. Average daily diet contains- 10-20mg of iron.
Absorption occurs all over the intestine, but more in the
upper part.
There are two major forms of dietary iron.
Heme iron, found primarily in red meats, is the most easily
absorbed form.
Majority of dietary iron is in ferric form.
It is reduced to ferrous form before absorption.
Absorption occurs through 2 separate iron transporters in
the intestinal mucosal cells.
Divalent metal transporter – 1 (DMT 1)
Ferroportin

15.  FACTORS FACILITATING FE ABSORPTION
Acid: By favouring dissolution and reduction of ferric form.
Reducing substances – Ascorbic acid.
Meat – By increasing Hcl secretionand providing heme iron.

FACTORS IMPEDING FE ABS
Alkalies – (Antacids) Renders iron insoluble, oppose its
reduction.
Phosphates (rich in egg yolk)
Phytates (maize, wheat) by complexing iron
Tetracyclines
Prescence of other foods in stomach.

16. It is a mechanism to prevent entry of excess iron in the body
Iron reaching inside mucosal cell is eigther transported to
plasma or oxidised to ferric form and complexed with
apoferritin to form ferritin.
The ferritin stored on the mucosal cells is lost when they are
shed (life span 2-4 days).
This is called ferritin curtain.
Thus the amount of iron entering into the body is governed
by the iron status of the body and the erythropoietic activity.

17. Free iron is highly toxic.
It is converted to ferric form and complexed with a
glycoprotein - transferrin (TF).
Iron is transported in to erythropoietic and other cells by
attachment of transferrin to transferrin receptors (TFRS)
which is engulfed by endocytosis.
Iron dissociates from complex and is utilised for Hb
synsthesis while TF and TFR return to cell surface to
carry fresh loads.

18. Iron is stored in reticulo endothelial cells in liver, spleen
bone morrow, also in hepatocytes & myocytes as ferritin
and haemosiderin.
Daily excretion – 0.5mg daily (adult male) mainly as
exfoliated G.I mucosal cells some RBC’s and in bile,
desquamated skin.
In menstruating women – monthly menstrual loss may be
averaged to 0.5-1 mg/day.
Excess iron is required during pregnancy for expansion of
RBC mass, transfer to foetus and loss during delivery
totaling about 700mg .

20. PREPARATIONS AND DOSAGE
Oral iron
This is the preferred route of iron administration.
Because
 Dissociable Ferrous salts are inexpensive.
Have high iron content
Better absorbed than ferric salts.
Some oral iron preparations
Ferrous sulphate – cheapest
Ferrous gluconate
Ferrous fumarate.
Colloidal ferric hydroxide
Ferric hydroxy poly maltose

21. Sustained release preperations – not rational.
Most of iron absorbed in upper intestine – but these
preperations release iron lower down.
Liquid formulations – may stain teeth.
Hence should be put back on tongue.
DOSE
A total of 200mg of elemental iron given daily in 3
divided doses – produce maximal haematopoietic
response.
Absorption of iron is much better when it is taken on
empty stomach – side effects are also more on empty
stomach.
Prophylactic dose – 30 mg iron daily.

22. PROPHYLATIC
pregnancy ,menstruation ,blood donors .
THERAPEUTIC
- to treat existing iron deficiency.
Nutritional deficiency.
Anaemia of infancy and pregnancy.
Anaemia due to acute or chronic blood loss.
menorrhagia ,peptic ulcer, hookworm infestation.

23. ADVERSE EFFECTS OF ORAL IRON
Adverse effects are related to elemental iron
content.
1.Epigastric pain
2.Heart burn
3.Nausea & vomiting
4.Staining of teeth
5.Metallic taste
6.Bloating, colic
7.Constipation

24. PARENTERAL IRON
 INDICATIONS
1.Oral iron is not tolerated - bowel upset is more.
2.Failure to absorb iron – mal absorption,
Inflammatory bowel disease.
3.Non compliance to oral iron.
4.In prescence of severe deficiency with chronic
bleeding.
Parenteral iron therapy needs calculation of the total
iron requirement of the pt.
Iron requirement (mg) = 4.4 X body wt (kg) X Hb
deficit (g/dl)

25.  PREPARATIONS:
IRON DEXTRAN for IM\IV use {imferon} contra
indicated in early pregnancy.
IRON SORBITOL CITRIC ACID COMPLEX{JECTOFER} for
IM injection
(urine turns black –iron sulfide formation).

26. IRON CARBOHYDRATE COMPLEX {UNIFERON}
- iron ,dextran sorbitol citric acid .
- Given IM , each ml contains 50 mg of elemental
iron.
Injection made by Z technique.

Test dose of 25 mg is given followed by 100 mg .
IV infusion is given at the rate of 10 drops per
minute.

27. Iron dextran
Ferrous –sucrose
 Sodium ferric gluconate
After a test dose with 0.5ml, 2ml to be given over
10min.
Alternatively dose diluted in 500ml glucose/saline –
to be infused over 6-8hrs.
Should be stopped if pt complains of giddiness,
paraesthesias and tightness in the chest.

28. ADVERSE EFFECTS OF PARENTERAL IRON
LOCAL –
pain at injection site
pigmentation of skin,
sterile abscess.
SYSTEMIC –
fever,
head ache,
joint pains,
flushing,
palpitation,
chest pain,
dyspnoea,
lymphnode enlargement.

29. IRON DEFICIENCY ANEMIA

 Most imp indication for medicinal iron.
CAUSES:
1.Nutritional deficiency
2.Chronic bleeding from G.I tract (common cause)
(ulcers, hook worm infestation)
3.Repeated attacks of malaria.
4.Chr. inflammatary diseases.

30. A rise in Hb level by 0.5 – 1g/dl per week is an
optimum response to iron therapy
It takes 1-3 months – depending on severity to
correct anemia and 2-3 months to replenish stores-
because after correction of anemia iron absorption
is slow.
 MEGALOBLASTIC ANEMIA
AS AN ASTRINGENT – ferric chloride – used in throat
paint.

31. ACUTE IRON POISONING
It occurs mostly in infants and children.
10-20 iron tablets or equivalent of the liquid
preperation (>60mg/kg iron) may cause serious
toxicity.
Very rare in adults.

32. Manifestations
Vomiting
Abdominal pain
Haemetemesis
Diarrhoea
Cyanosis
Lethargy
Dehydration
Acidosis
Convulsions & finally shock
Cardio vascular collapse.

33. Treatment – should be prompt
1)To prevent further absorption of iron from the gut.
Induce vomiting / perform gastric lavage with sod.
Bicarbonate sol- To render iron insoluble.
Give egg yolk and milk orally- To complex iron
Activated charcoal does not absorb iron.
1)To bind and remove already absorbed iron.
Desferroxamine (an iron chelating apent) – is the IM –
0.5-1g repeated 4-12 hrly.
DTPA or calcium edetate – also used.
1)Supportive measures
Fluid electrolyte balance maintained.
Acidosis corrected by IV infusion

34.  It occurs in pts with chronic infections (TB),
Inflammatory disease (rheumatoid arthritis), cancer,
trauma.
Hypoferrimia, in presence of bone marrow iron
overload is a constant feature.
There is deficient delivery of iron to developing RBC.
Anaemia does not respond to iron therapy.

35. Epoetin a&b has molecular weight 36,000.
It is synthesized by kidney in response to hypoxemia.
Given by IV route.
 Plasma half life is - 6-8 HRS.
 Adverse Effects:
- Hypertension, rise in hematocrit values..

36. Anaemia of end stage renal failure.
To permit autologous blood transfusion.
Anemia due to anticancer drugs and HIV infection.