3. • HAEMATINICS are substances required in the
formation of blood, and are used for treatment of
anaemias.
• Anaemia occurs when the balance between production
and destruction of RBCs is disturbed by:
(a) Blood loss (acute or chronic)
(b) Impaired red cell formation due to:
• Deficiency of essential factors, i.e. iron, vitamin B12 &
folic acid.
• Bone marrow depression (hypoplastic anaemia),
erythropoietin deficiency.
(c) Increased destruction of RBCs (haemolytic anaemia)
3
4. 1. Normocytic, normochromic anaemia:
Acute blood loss
2. Microcytic, hypochromic anaemia
Iron deficiency anaemia, thalessimia
3. Macrocytic anaemia
Vit B12 deficiency, folic acid deficiency
4. Pernicious anaemia
Vit B12 deficiency
5. Hemolytic anaemia
Destruction of RBC
6. Sickle cell anaemia
Sickle shaped RBC
7. Aplastic anaemia
Bone marrow disorder
Types of Anaemia
4
5. • IRON is an essential body constituent. It is an essential
constituent of hemoglobin, cytochrome, and other components
of respiratory enzyme systems. Its chief functions are in the
transport of oxygen to tissue (hemoglobin) and in cellular
oxidation mechanisms. Depletion of iron stores may result in
iron-deficiency anemia. Iron is used to build up the blood in
anemia.Total body iron in an adult is 2.5–5 g. It is more in men
(50 mg/kg) than in women (38 mg/kg). It is distributed into:
• Haemoglobin (Hb) : 66%
• Iron stores as ferritin and haemosiderin: 25%
• Myoglobin (in muscles) : 3%
• Parenchymal iron (in enzymes, etc.) : 6%
5
7. • Haemoglobin is a protoporphyrin; each molecule
having 4 iron containing haeme residues. It has
0.33% iron; thus loss of 100 ml of blood (containing
15 g Hb) means loss of 50 mg elemental iron. To
raise the Hb level of blood by 1 g/dl—about 200 mg
of iron is needed. Iron is stored only in ferric form,
in combination with a large protein apoferritin.
7
8. Iron is found in two forms:
• Heme Iron: Meat, Myoglobin
• Non-Heme Iron: Cereals, Fruits, Legumes
Vitamin C increases absorption of Non-Heme Iron
Iron is absorbed via two mechanisms:
i) active transport of ferrous iron and
ii) absorption of iron complexed with heme
8
10. • MOA: Iron is important component of hemoglobin that carries
oxygenated blood from lungs to different body parts. It also acts
as catalyst for many metabolic reactions essential for cell growth.
It maintains a healthy immune system & aids in energy
production. It is transported inside mucosal cell by DMT1 &
across basolateral membrane BY FP1 transporter protein . Iron
released into plasma binds to transferrin & transported to
different cells.
• Indication:
• Dietary Iron deficiency
• Pregnancy
• Premature babies
• Malabsorption
• Haemodialysis
• Anaemia
10
11. Oral iron
• The preferred route of iron administration is oral.
• Ferrous sulfate: (hydrated salt 20% iron, dried salt 32% iron)
• Ferrous gluconate (12% iron)
• Ferrous fumarate (33% iron)
Dose: 200 mg elemental iron (infants and children 3–5 mg/kg) TDS Absorption
is much better in empty stomach.
A/E: Gastric Irritaion, Constipation, Staining of teeth, Metallic taste
Parenteral iron
• Iron therapy by injection is indicated only when:
1. Oral iron is not tolerated: bowel upset is too much.
2. Failure to absorb oral iron: inflammatory bowel disease.
3. Non-compliance to oral iron.
4. In presence of severe deficiency with chronic bleeding.
5. Along with erythropoietin.
• IRON DEXTRAN
• IRON SUCROSE, DOSE: 75mg i.m (Max 100mg i.m.)
11
12. ACUTE IRON POISONING
• It occurs mostly in infants and children: 10–20 iron tablets or
equivalent of the liquid preparation (> 60 mg/kg iron) may cause
serious toxicity in them.
• Manifestations are vomiting, abdominal pain, haematemesis,
diarrhoea, lethargy, cyanosis, dehydration, acidosis, convulsions;
finally shock, cardiovascular collapse and death.
• Treatment It should be prompt.
Toprevent further absorption of iron from gut
(a)Induce vomiting or perform gastric lavage
(b) Give egg yolk and milk orally: to complex iron.
To bind and remove iron already absorbed Desferrioxamine (an
iron chelating agent) is the drug of choice. It should be injected
i.m. (preferably) 0.5–1 g (50 mg/kg) repeated 4–12 hourly as required,
or i.v. (if shock is present) 10–15 mg/kg/hour; max 75 mg/kg in a day
till serum iron falls below 300 μg/dl.
12
14. VITAMIN B12 (COBALAMIN)
• It occurs as red crystals synthesized in nature only by
microorganisms; plants and animals acquire it from
them.
• MOA: Vitamin B12 is essential constituents of the
human diet, being necessary for DNA synthesis and
consequently for cell proliferation.
• Vitamin B12 is important in the normal functioning of
the nervous system due to its role in the synthesis of
myelin and in the maturation of developing red blood
cells in the bone marrow.
• Dietary sources Liver, kidney, sea fish, egg yolk, meat,
cheese, legumes, etc.
• Daily requirement 1–3 μg, pregnancy and lactation 3–
5 μg.
14
15. Vitamin B12 is a family of related compounds
containing a cobalt atom (cobalamins).
The two dietary forms of vitamin B12 are available and they are
known as methylcobalamin (methyl-B12) and 5-
deoxyadenosylcobalamin (coenzyme-B12).
Synthetic forms of vitamin B12 are known as hydroxy-cobalamin
and cyanocobalamin (not occur naturally in foods).
15
16. VITAMIN B12 IS REQUIRED
FOR:
16
A. Conversion of methyl-FH4 to active formyl-FH4, which
is a co-factor in the synthesis of purines and
pyrimidines.
B. Isomerisation of methylmalonyl-CoA to succinyl-CoA.
17. • METHYLCOBALAMIN is the active coenzyme form
of vit B12 for synthesis of methionine and S-
adenosylmethionine.
• This preparation of vit B12 in a dose of 1.5 mg/day has
been especially promoted for correcting the
neurological defects in diabetic, alcoholic and other
forms of peripheral neuropathy.
• Indications:
a) Megaloblastic anemia
b) Neurologic syndrome associated with cobalamin
deficiency
c) Pernicious anemia
d) Treatment of vit B12 deficiency
17
20. Folate deficiency occurs due to:
(a) Inadequate dietary intake
(b) Malabsorption: especially involving upper intestine—coeliac disease, tropical
sprue, regional ileitis, etc.
(c) Biliary fistula; bile containing folate for recirculation is drained.
(d) Chronic alcoholism: intake of folate is generally poor.
(e) Increased demand: pregnancy, lactation, rapid growth periods, haemolytic
anaemia and other diseases.
(f) Drug induced: prolonged therapy with anticonvulsants (phenytoin,
phenobarbitone, primidone) and oralcontraceptives— interfere with absorption and
storage of folate.
Manifestations of deficiency are:
(i) Megaloblastic anaemia, indistinguishable from that due to vit B12 deficiency.
(ii) Epithelial damage: glossitis, enteritis, diarrhoea, steatorrhoea.
(iii) Neural tube defects, including spina bifida in the offspring, due to maternal
folate deficiency. 20
21. SOURCES : YEAST , LIVER , GREEN VEGETABLES, FRUITS , NUTS
AND CEREALS
DAILY REQUIREMENTS : ADULT: 50 MCG/ DAY PREGNANT
WOMEN : 100-200 MCG / DAY
LACTATING WOMEN : 100-200 MCG / DAY
DOSE: THERAPEUTIC 2 TO 5 MG/DAY, PROPHYLACTIC 0.5
MG/DAY. INDICATIONS:
TREAT MAGALOBLASTIC ANEMIA DUE TO FOLATE DEFICIENCY
PREGNANT WOMEN
PREMATURE INFANTS
PATIENTS WITH HEMOLYTIC ANEMIA
METHOTREXATE TOXICITY
CITROVORUM FACTOR RESCUE
ENHANCE ANTICANCER EFFICACY OF 5-FLUOROURACIL
WITH ANTICONVULSANT DRUGS 21
22. ERYTHROPOIETIN IS A GLYCOPROTEIN, NORMALLY
MADE BY THE KIDNEYS, THAT REGULATES RED BLOOD CELL
PROLIFERATION AND DIFFERENTIATION IN BONE MARROW.
(A)STIMULATES PROLIFERATION OF COLONY FORMING
CELLS. (B)INDUCES HAEMOGLOBIN FORMATION
& ERYTHROBLAST
MATURATION.
(C)RELEASES RETICULOCYTES IN THE CIRCULATION.
THE RECOMBINANT HUMAN ERYTHROPOIETIN (EPOETIN Α,
Β) IS ADMINISTERED 25–100 U/KG BY I.V. OR S.C.
INJECTION 3 TIMES A WEEK.
22
23. Indication:
• Anaemia
• Chronic Renal failure
(patients with Hb ≤ 8 g/dl should be considered for EPO)
• Anaemia in AIDS patients treated with zidovudine.
• Cancer chemotherapy induced anaemia.
• Preoperative increased blood production
for autologous transfusion during surgery.
• A/E: Increased clot formation in the A-V shunts,
hypertensive episodes, serious thromboembolic
events, occasionally seizures & Flu like symptoms.23
