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PRESENTED BY:-
Mr.DEEPAK B. GADHAVE
B.PHARM B-pharm viiTH
GUIDED BY:-Dr. S. V.TEMBHURNE
H.O.D. OF PHARMACOLOGY
S.N.I.O.PHARMACY PUSAD
HAEMATINICS:-Thes are the agent required in the
formation of blood & used for treatment of anemia's.
Etiology:-Anaemia occurs when,
A. Blood loss (acute or cronic)
B. Impaired red formation due to;
a)Deficiency of iron,vit.B12. folic acid.
b)Bon marrow dipression.
C. Increased destruction of RBCs.
Classification:-
1. Iron & it’s compound:-
eg:-ferrous succinat, ferrous sulfate, ferrous
gluconate etc.
2. Maturation factor:-
eg:-cynocobalamine, Hydroxycynocobalamine.
3. Miscellaneous:-
eg:-copper, cobalt,Riboflavine.
According to Greek thought MARS is the god of
strength & IRON is dedicated to it.
 Source of iron:-
Rich:- Liver, egg yolk, dry bean, dry fruit.
Medium:- Meat, chicken, fish, banana, apple.
Poor:- Milk & it’s product.
 Daily requirement:-
Adult male :- 0.5-1mg(13µg/kg).
Adult female:-1-2mg(21µg/kg).
Infant :-60µg/kg.
Children :-25µg/kg.
Pregnancy :-3-5mg(80µg/kg).
Iron absorption
 Its absorption occurs all over the intestine.
 In the stomch containing HCL & reducing agent are convert the ferric
to ferrous.
 Two separate iron transporters in the intestinal mucosal cells
function to effect iron absorption.
 At the luminal membrane the divalent metal transporter 1 (DMT1)
carrys ferrous iron into the mucosal cell.
 The ferroportin are bound with ferrous iron & pass through mucosal
cell directly into the blood steam.
Factor affecting absorption:-
1. Achlorhydriya
2. Alkline pH
3. Presence of food in stomach
4. Complex with tetracyclin & phosphate
Transport, utilization, storage and excretion
 As such, on entering plasma it is immediately converted to the
ferric form and complexed with a glycoprotein transferrin (Tf).
 Iron is transported into erythropoietic and other cells through
attachment of transferrin to specific membrane bound
transferrin receptors(T f 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 haemoglobin synthesis or other
purposes.
 Tf and T f R are returned to the cell surface to carry fresh
loads.
Storage:-
1. Reticulo endothelial cell in liver.
2. Spleen
3. Bone marrow
4. hepatocytes and myocytes
Exreation:-
 Daily excretion in adult male is 0.5–1 mg, mainly
g.i. mucosal cells, some RBCs and in bile from faeces.
 Other routes are skin, very little in urine and sweat.
 In menstruating women, monthly menstrual loss may be
averaged to 0.5–1 mg/day.
Adverse effects :-
1. Epigastric pain.
2. heartburn.
3. nausea, vomiting.
4. staining of teeth.
5. metallic taste.
6. Constipation.
Preparations and dose:-
1. Ferrous succinate
2. Iron choline citrate
3. Ferric ammonium citrate
4. Ferric gluconate
5. Ferrous fumarat
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: malabsorption.
3. Non-compliance to oral iron.
4. In presence of severe deficiency with chronic bleeding.
5. Along with erythropoietin
preparations for parenteral use are:
(i) Iron- dextran.
(ii) Iron-sorbitol-citric acid
Therapeutic use:-
1. Iron deficiency anaemia.
2. Megaloblastic anaemia.
3. As an astringent :-Ferric chloride is used in
throat paint.
Miscellaneous:-
Copper :-
 Haeme synthesis is interfered in copper Deficiency.
 Dose 0.5–5 mg of copper sulphate.
Cobalt:-
It stimulates erythropoiesis transiently,
probably by inducing tissue hypoxia → increased
erythropoietin production.
Riboflavin :- Hypoplastic anaemia occurs
in riboflavin deficiency
MATURATION FACTORS
VITAMIN-B12 (Cyanocobalamin)
1. Vit B12 occurs as water soluble, thermostable
red crystals.
2.It is synthesized in nature only by microorganisms;
plants and animals acquire it from them.
Dietary sources :-Liver, kidney, sea fish, egg yolk, meat,
cheese.
Daily requirement: 1–3 μg, pregnancy and lactation
3–5 μg.
Metabolic functions:-
 Vit B12 is essential for the conversion of hom
o-cysteine to methionine.
 Purine and pyrimidine synthesis .
 .
 Now it appears that interference with the
reaction:-
 Vit B12 is essential for cell growth and
multiplication.
Utilization of vit B12 . :-
 Intrinsic factor secreted by stomach forms a complex with
B12 attaches to specific receptors present on intestinal
mucosal cells and is absorbed by active carrier mediated
transport.
 Vit B12 is transported in blood in combination with a
specific β globulin transcobalamin II (TCII).
 Vit B12 is especially taken up by liver cells and stored about
2/3 to 4/5 of body’s content (2–8 mg) is present in liver.
 Vit B12 is not degraded in the body. It is excreted mainly in
bile (3–7 μg/day); all but 0.5–1 μg of this is reabsorbed—
considerable entero-hepatic circulation occurs.
 the absence of intrinsic factor or when there is
malabsorption.
 From parentral rout (i.m/s.c) is mainly excreated
via urin.
Deficiency:-
 Pernicious anaemia.
 Other cause of gastric mucosal damage.
 Malabsorption.
 Nutritional deficiency
Manifestations of deficiency are:-
 Megaloblastic anaemia
 g.i. disturbances
 Neurological degeneration.
 Preparations, dose, administration:-
Cyanocobalamin:- MACRABIN 35 μg/5ml
Hydroxocobalamin: -REDISOL-H,
Methylcobalamin:-METHYLCOBAL 0.5 mg tab.
Therapeutic use:-
 Pernicious anaemia.
 Malabsorption syndroms.
 Nutritional deficiency.
 Neurological condition.
 Psychitric disorder.
Adevrs drug reaction:-
Allergic reactions have occurred by
injection
FOLIC ACID
Folic acid(Pteroyl glutamic acid) is a member of
the B complex group of vitamine.
Dietary sources:-
Liver, green leafy vegetables (spinach),
egg, meat, milk.
Daily requirement:- 0.2 mg/day
Utilization:-
 Folic acid is present in food as poly-glutamates
 The additional glutamate residues are
split off primarily in the upper intestine before being
absorbed.
 Reduction to DHFA and methylation also occurs at this site.
 It is transported in blood mostly as methyl-THFA which is
partly bound to plasma proteins.
 Small, physiological amounts of folate are absorbed by
specific carrier-mediated active transport in the intestinal
mucosa.
 Folic acid is rapidly extracted by tissues and stored in cells as
polyglutamate.
 Liver takes up a large part and secretes methyl-THFA in bile
& again reabsorbed by enterohepatic cycle
 50-90% of adose may be excreated in urin.
Metabolic functions
1. Conversion of homocysteine to methionine:
2. Generation of thymidylate, an essential
constituent of DNA:
3. Conversion of serine to glycine.
4. Purine synthesis.
5. Histidine metabolism.
Deficiency & menifestation:-
1. Megaloblastic anaemia.
2. Nutritional deficiency.
3. Malabsorption.
4. Epithelial damage.
5. Weight loss.
Therapeutic use:-
1. Megaloblastic anaemia.
2. Improve absorpton.
3. Protect epithelial cell.
4. Groth factor.
Adverse effects:-
Hypersesitivity reaction occor by injection.
Preparations and dose
1. Folic acid: -liqid oral.
2. Injectabale.
3. Folinic acid:-CALCIUM LEUCOVORIN 3
mg/ml inj.
These are high molecular weight substances
which exert colloidal osmotic (oncotic)pressure,
and when infused i.v. retain fluid in the vascular
compartment.
They are used to correct hypo-volemia due
to loss of plasma/blood.
Ideal properties of a plasma expander are:
1. Should exert oncotic pressure comparable to plasma.
2. Should remain in circulation and not leak out in tissues.
3. Should be pharmacodynamically inert.
4. Should not be pyrogenic or antigenic.
5. Should be stable, easily sterilizable.
Dextran
It is a polysaccharide obtained from sugar
beat .
Dextran-70
The more commonly used preparation is dextran-
70.
 It expands plasma volume for nearly 24 hours.
 it is slowly excreted by glomerular filtration as well
as oxi-dized in the body over weeks.
 Some amount is deposited in RE cells.
 Dextran has nearly all the properties of an
ideal plasma expander.
Dextran-40
 It acts more rapidly than dextran-70.
 It reduces blood viscosity.
 Microcirculation may improve.
Polyvinyl pyrrolidone (PVP)
 It is a synthetic polymer (average MW 40,000) used as a 3.5%
solution.
 It interferes with blood grouping and cross-matching and is a
histamine releaser.
 PVP is slowly excreted by kidney and small amounts by liver
into bile.
 It is stored in RE cell.
USE OF PLASMA EXPANDERS:-
1. Plasma loss.
2. Burn
3. Hypovolemic & endotoxin shock.
4. Sever trauma & extensiv tissu damage
5. Whole blood loss.
Contraindications
1. severe anaemia.
2. cardiac failure.
3. Pulmonary edema.
Haematinics

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Haematinics

  • 1. PRESENTED BY:- Mr.DEEPAK B. GADHAVE B.PHARM B-pharm viiTH GUIDED BY:-Dr. S. V.TEMBHURNE H.O.D. OF PHARMACOLOGY S.N.I.O.PHARMACY PUSAD
  • 2.
  • 3. HAEMATINICS:-Thes are the agent required in the formation of blood & used for treatment of anemia's. Etiology:-Anaemia occurs when, A. Blood loss (acute or cronic) B. Impaired red formation due to; a)Deficiency of iron,vit.B12. folic acid. b)Bon marrow dipression. C. Increased destruction of RBCs.
  • 4. Classification:- 1. Iron & it’s compound:- eg:-ferrous succinat, ferrous sulfate, ferrous gluconate etc. 2. Maturation factor:- eg:-cynocobalamine, Hydroxycynocobalamine. 3. Miscellaneous:- eg:-copper, cobalt,Riboflavine.
  • 5. According to Greek thought MARS is the god of strength & IRON is dedicated to it.  Source of iron:- Rich:- Liver, egg yolk, dry bean, dry fruit. Medium:- Meat, chicken, fish, banana, apple. Poor:- Milk & it’s product.  Daily requirement:- Adult male :- 0.5-1mg(13µg/kg). Adult female:-1-2mg(21µg/kg). Infant :-60µg/kg. Children :-25µg/kg. Pregnancy :-3-5mg(80µg/kg).
  • 6. Iron absorption  Its absorption occurs all over the intestine.  In the stomch containing HCL & reducing agent are convert the ferric to ferrous.  Two separate iron transporters in the intestinal mucosal cells function to effect iron absorption.  At the luminal membrane the divalent metal transporter 1 (DMT1) carrys ferrous iron into the mucosal cell.  The ferroportin are bound with ferrous iron & pass through mucosal cell directly into the blood steam. Factor affecting absorption:- 1. Achlorhydriya 2. Alkline pH 3. Presence of food in stomach 4. Complex with tetracyclin & phosphate
  • 7.
  • 8. Transport, utilization, storage and excretion  As such, on entering plasma it is immediately converted to the ferric form and complexed with a glycoprotein transferrin (Tf).  Iron is transported into erythropoietic and other cells through attachment of transferrin to specific membrane bound transferrin receptors(T f 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 haemoglobin synthesis or other purposes.  Tf and T f R are returned to the cell surface to carry fresh loads.
  • 9.
  • 10. Storage:- 1. Reticulo endothelial cell in liver. 2. Spleen 3. Bone marrow 4. hepatocytes and myocytes Exreation:-  Daily excretion in adult male is 0.5–1 mg, mainly g.i. mucosal cells, some RBCs and in bile from faeces.  Other routes are skin, very little in urine and sweat.  In menstruating women, monthly menstrual loss may be averaged to 0.5–1 mg/day.
  • 11. Adverse effects :- 1. Epigastric pain. 2. heartburn. 3. nausea, vomiting. 4. staining of teeth. 5. metallic taste. 6. Constipation. Preparations and dose:- 1. Ferrous succinate 2. Iron choline citrate 3. Ferric ammonium citrate 4. Ferric gluconate 5. Ferrous fumarat
  • 12. 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: malabsorption. 3. Non-compliance to oral iron. 4. In presence of severe deficiency with chronic bleeding. 5. Along with erythropoietin preparations for parenteral use are: (i) Iron- dextran. (ii) Iron-sorbitol-citric acid
  • 13. Therapeutic use:- 1. Iron deficiency anaemia. 2. Megaloblastic anaemia. 3. As an astringent :-Ferric chloride is used in throat paint.
  • 14. Miscellaneous:- Copper :-  Haeme synthesis is interfered in copper Deficiency.  Dose 0.5–5 mg of copper sulphate. Cobalt:- It stimulates erythropoiesis transiently, probably by inducing tissue hypoxia → increased erythropoietin production. Riboflavin :- Hypoplastic anaemia occurs in riboflavin deficiency
  • 15. MATURATION FACTORS VITAMIN-B12 (Cyanocobalamin) 1. Vit B12 occurs as water soluble, thermostable red crystals. 2.It is synthesized in nature only by microorganisms; plants and animals acquire it from them. Dietary sources :-Liver, kidney, sea fish, egg yolk, meat, cheese. Daily requirement: 1–3 μg, pregnancy and lactation 3–5 μg.
  • 16. Metabolic functions:-  Vit B12 is essential for the conversion of hom o-cysteine to methionine.  Purine and pyrimidine synthesis .  .
  • 17.  Now it appears that interference with the reaction:-  Vit B12 is essential for cell growth and multiplication.
  • 18. Utilization of vit B12 . :-  Intrinsic factor secreted by stomach forms a complex with B12 attaches to specific receptors present on intestinal mucosal cells and is absorbed by active carrier mediated transport.  Vit B12 is transported in blood in combination with a specific β globulin transcobalamin II (TCII).  Vit B12 is especially taken up by liver cells and stored about 2/3 to 4/5 of body’s content (2–8 mg) is present in liver.  Vit B12 is not degraded in the body. It is excreted mainly in bile (3–7 μg/day); all but 0.5–1 μg of this is reabsorbed— considerable entero-hepatic circulation occurs.
  • 19.  the absence of intrinsic factor or when there is malabsorption.  From parentral rout (i.m/s.c) is mainly excreated via urin. Deficiency:-  Pernicious anaemia.  Other cause of gastric mucosal damage.  Malabsorption.  Nutritional deficiency Manifestations of deficiency are:-  Megaloblastic anaemia  g.i. disturbances  Neurological degeneration.
  • 20.  Preparations, dose, administration:- Cyanocobalamin:- MACRABIN 35 μg/5ml Hydroxocobalamin: -REDISOL-H, Methylcobalamin:-METHYLCOBAL 0.5 mg tab. Therapeutic use:-  Pernicious anaemia.  Malabsorption syndroms.  Nutritional deficiency.  Neurological condition.  Psychitric disorder. Adevrs drug reaction:- Allergic reactions have occurred by injection
  • 21. FOLIC ACID Folic acid(Pteroyl glutamic acid) is a member of the B complex group of vitamine. Dietary sources:- Liver, green leafy vegetables (spinach), egg, meat, milk. Daily requirement:- 0.2 mg/day
  • 22. Utilization:-  Folic acid is present in food as poly-glutamates  The additional glutamate residues are split off primarily in the upper intestine before being absorbed.  Reduction to DHFA and methylation also occurs at this site.  It is transported in blood mostly as methyl-THFA which is partly bound to plasma proteins.  Small, physiological amounts of folate are absorbed by specific carrier-mediated active transport in the intestinal mucosa.  Folic acid is rapidly extracted by tissues and stored in cells as polyglutamate.  Liver takes up a large part and secretes methyl-THFA in bile & again reabsorbed by enterohepatic cycle  50-90% of adose may be excreated in urin.
  • 23. Metabolic functions 1. Conversion of homocysteine to methionine: 2. Generation of thymidylate, an essential constituent of DNA: 3. Conversion of serine to glycine. 4. Purine synthesis. 5. Histidine metabolism.
  • 24. Deficiency & menifestation:- 1. Megaloblastic anaemia. 2. Nutritional deficiency. 3. Malabsorption. 4. Epithelial damage. 5. Weight loss. Therapeutic use:- 1. Megaloblastic anaemia. 2. Improve absorpton. 3. Protect epithelial cell. 4. Groth factor.
  • 25. Adverse effects:- Hypersesitivity reaction occor by injection. Preparations and dose 1. Folic acid: -liqid oral. 2. Injectabale. 3. Folinic acid:-CALCIUM LEUCOVORIN 3 mg/ml inj.
  • 26.
  • 27. These are high molecular weight substances which exert colloidal osmotic (oncotic)pressure, and when infused i.v. retain fluid in the vascular compartment. They are used to correct hypo-volemia due to loss of plasma/blood.
  • 28. Ideal properties of a plasma expander are: 1. Should exert oncotic pressure comparable to plasma. 2. Should remain in circulation and not leak out in tissues. 3. Should be pharmacodynamically inert. 4. Should not be pyrogenic or antigenic. 5. Should be stable, easily sterilizable. Dextran It is a polysaccharide obtained from sugar beat .
  • 29. Dextran-70 The more commonly used preparation is dextran- 70.  It expands plasma volume for nearly 24 hours.  it is slowly excreted by glomerular filtration as well as oxi-dized in the body over weeks.  Some amount is deposited in RE cells.  Dextran has nearly all the properties of an ideal plasma expander. Dextran-40  It acts more rapidly than dextran-70.  It reduces blood viscosity.  Microcirculation may improve.
  • 30. Polyvinyl pyrrolidone (PVP)  It is a synthetic polymer (average MW 40,000) used as a 3.5% solution.  It interferes with blood grouping and cross-matching and is a histamine releaser.  PVP is slowly excreted by kidney and small amounts by liver into bile.  It is stored in RE cell.
  • 31. USE OF PLASMA EXPANDERS:- 1. Plasma loss. 2. Burn 3. Hypovolemic & endotoxin shock. 4. Sever trauma & extensiv tissu damage 5. Whole blood loss. Contraindications 1. severe anaemia. 2. cardiac failure. 3. Pulmonary edema.