2. Haematinics are the substance required in the formation of
blood and are used for the treatment of Anaemia
HAEMATINICS
Destruction of Red
blood cells
Production of Red
blood cells
Anaemia
2
3. Microcytic anaemia : deficiency of Iron
Macrocytic anaemia : deficiency of vit.B12 and
folic acid
Pernicious anaemia : lack of intrinsic factor
Aplastic anaemia : due to bone marrow
dysfunction
Haemolytic anaemia : excessive haemolysis
Sickle cell anaemia : sickle shaped RBCs
HAEMATINICS (TYPES OF ANAEMIA)
3
4. Blood loss
Acute OR
Chronic
Deficiency of essential
factors : Iron, Vit B12,
Folic acid and Bone
marrow depression
Increased
destruction of
RBCs
HAEMATINICS
Imbalance between
Production and
destruction of
RBCs
4
5. HAEMATINICS (IRON)
Haemoglobin : 66%
Ferritin and
haemosiderin : 25%
Myoglobin (in
muscles) : 3%
Parenchymal iron
(in enzymes) : 6%
1) Iron : Essential body constituent
Total body iron requirement in healthy human is 12– 16
mg/kg and in premenopausal women 18mg/kg
Iron is stored only in ferric form, in combination with larger protein
Apoferritin
Apoferritin + Fe3+ Ferritin Haemosiderin
aggregates
5
6. HAEMATINICS (IRON)
Poor sources:
milk and its
products, root
vegetables
Medium
sources: meat,
chicken, fish,
spinach,
banana, apple
Rich sources :
liver, egg yolk,
oyster, dry
fruits, dry
beans, wheat
germ, yeast
Dietary source of iron
6
7. 1 Hb = 4 protein chain(globin) + 4 Haeme moiety
Haeme consist of tetrapyrrole porphyrine ring contains
ferrous ion (Fe2+)
HAEMATINICS (HAEMOGLOBIN MOLECULE)
7
141
amino
acid
146
amino
acid
9. Absorption occurs in all over the intestine but mostly in upper
part of small intestine (duodenum)
Major part of dietary ion is inorganic and present in ferric form
that need to be reduced to ferrous ion before absorption.
2 ion transporters present in intestinal mucosal cells –
DMT1(divalent metal transporter1)
FP (ferroportin)
DMT1 – transports ferrous ion into mucosal cells
FP – iron released from the haeme is transported across the
basolateral membrane
DCYTB – duodenal cytochrome b
HAEMATINICS (ABSORPTION OF IRON)
9
10. Acid : by favoring dissolution and reduction of ferric
iron
Reducing substances : ascorbic acid, amino
acids will reduce ferric iron and make absorbable
form
Meat : by increasing HCL secretion and providing
haeme iron
HAEMATINICS (FACTORS FACILLITATING IRON ABSORPTION)
10
11. Mechanism that prevents entry of excess iron into the body
Iron reaching inside mucosal cell is either transported to
blood OR oxidised to ferric form that will make a complex
with apoferritin to form ferritin
Ferritin is stored in mucosal cells and it is lost when they are
shed (life span 2-4 days) – ferritin curtain
During iron deficiency – larger % of iron will be entered into
blood circulation from the stored iron
When erythropoesis is occuring briskly OR when body iron
is low – iron is transported to the blood from ferritin storage
HAEMATINICS (MUCOSAL BLOCKING OF IRON)
11
13. On entering plasma, free iron is converted into ferric form
and complexed with glycoprotein transferrin(Tf)
Iron is transported into erythropoetic and other cells through
attachment of Tf to specific memb bound Tf receptors(TfRs)
This complex is engulfed by receptor mediated endocytosis
Iron dissociated from the complex at acidic pH of intracellular
vesicles and released iron is utilized for hemoglobin
synthesis while Tf and TfR are return to carry fresh load
In the state of high erythropoesis – TfR in erythropoetic cells
are increased in number
HAEMATINICS (TRANSPORT AND UTILLIZATION OF IRON)
Free
iron
13
14. Iron stored in cells of liver, spleen, bonemarrow and myocytes in the
form of ferritin and hemosiderin after entering these cells through
TfRs
Apoferritin synthesis is regulated by iron in the body
When apoferritin is high the Iron regulating element on mRNA is
blocked – transcription of apoferritin doesn’t occur
On other hand, more apoferritin is synthesized to trap iron when
iron stores are rich
HAEMATINICS (STORAGE AND EXCRETION OF IRON)
14
15. Plasma iron derived from destruction of old RBCs (120days
lifespan) and from intestinal absorption forms – that is
available for erythropoeisis and for restorage
Iron is excreted via various route – bile, faeces, urin, skin,
sweat
During monthly menstruation, women losses about 0.5 to 1
mg/day
Excess iron is required in preganancy to produce more
RBCs and transfer it to foetus and loss during delivery
15
HAEMATINICS (STORAGE AND EXCRETION OF IRON)
16. Other forms present in oral formulations are
• Ferrous succinate
• Iron choline citrate
• Iron calcium complex
• Ferric ammonium citrate
• Ferrous aminoate
• Ferric glycerophosphate
HAEMATINICS (ORAL PREPARATIONS OF IRON)
1) Ferrous sulfate : hydrated salt
20% iron, dried salt 32% iron
FEROSOLATE 200mg tab
cheapest
leaves metallic taste in mouth
2) Ferrous gluconate : 12% iron
FERRONICUM 300mg tab
Ferrous fumarate : 33% iron
Less water soluble that ferrous
sulfate and it is tasteless
3) Colloidal ferric hydroxide :
50% iron
NEOFERUM 200mg tab,
400mg/5ml liq.
16
17. Parenteral iron preparations –
Indicated parentally only when :
1) Oral iron is not tolerated, bowel upset is too much
2) Malabsorption, failure to absorb oral iron (IBD, RA
decreases the iron absorption and utillization rate)
3) In presence of severe deficiency with chronic bleeding
In above situations
Iron requirement(mg) = 4.4 * body weight(kg) * Hb (g/dl)
HAEMATINICS (PARENTERAL PREPARATIONS OF IRON)
17
18. 1) Iron dextran –
High mol weight
Can be given i.m. or i.v.
i.m. absorbed through
lymphatics
Taken up by macrophages and
made slowly available to
erythron
2) Iron-sorbitol citric acid –
Low mol weight
i.m. use
Absorbed directly into
circulation
Directly available
18
HAEMATINICS (PARENTERAL PREPARATIONS OF IRON)
19. Adverse effect of parenteral iron :
local pain at site of injection, pigmentation of skin
Fever, headache, joint pain, lymph node enlargement
Adverse effect of oral iron :
Epigastric pain, heart burn, nausea, blotting,
constipation due to alteration of intestinal flora
These effects are differ in individuals
19
HAEMATINICS (ADVERSE EFFECT OF IRON PREPARATIONS)
21. Cyanocobalamin and hydroxocobalamin
Vitamin B12 will causes the pernicious anaemia and it takes
2-3 years to develop
Water soluble, Thermo stable red crystals
Synthesized in nature (by micro organism, plants, animals)
Daily requirement : 2-3 mcg, 4-5 mcg in pregnancy and
lactation
Dietary sources : meat, eggs, dairy products
HAEMATINICS (VITAMIN B12)
21
23. All cobalamin must be converted into its active form, methyl-
cobalamin OR 5-deoxyadenosyl cobalamin for activity in the
body
Absorption of vitB12 requires an intrinsic factor which form
direct complex with vitB12
Healthy stomach secretes a large excess of intrinsic factor,
vitB12 complex with intrinsic factor
Complex attached to specific receptors present on intestinal
mucosal cells and absorbed by active transport (distal ileum)
VitB12 is transported in blood in combination with trans-
cobalamin II (TCII)
VitB12 is taken up by liver cells and stored in hepatocytes
HAEMATINICS (UTILLIZATION OF VITAMIN B12)
23
24. Thus, in absence of intrinsic factor and during
malabsorption – vit B12 deficiency occurs rapidly
VitB12 is completely absorbed after i.m or s.c injection
VitB12 is not degraded in body, it is excreted in bile
Normally traces are excreted in urine but when it it given
>100mg parenterally, a large part is excreted in urine,
because plasma protein binding sites gets saturated amd free
vitB12 is filtered through glomerulus
HAEMATINICS (UTILLIZATION OF VITAMIN B12)
24
25. VitB12 deficiency occur due to :
1) Addisonian pernicious anaemia – autoimmune disorder,
which results in destruction of gastric parietal cells, absence of
intrinsic factor, inability to absorb vitB12
2) Gastric mucosal damage – Gastric carcinoma, gastrectomy,
chronic gastritis
3) Malabsorption
4) Consumption of intestinal vitB12 by abnormal flora in
intestine (blind loop syndrome)
5) Increased demand – pregnancy, infancy
HAEMATINICS (DEFFICIENCY OF VITAMIN B12)
25
26. VitB12 deficiency :
1-5 mg of oral tab of vitB12, improves appetite, patient
feels better, mucosal lesion heal in 1-2 weeks, Hb and
hematocrit increases progressively, complete recovery time
depends on severity of disease
Mega doses of VitB12 :
It is given in neuropathies, psychiatric disorders,
cutaneous sarcoid, fatigue
Tobacco amblyopia :
Impairment of vision, visual field defects and hindered
central vision
HAEMATINICS (USES OF VITAMIN B12)
26
28. Vitamin B9
Chemical name – Pteroyl glutamic acid (PGA) consists of
pteridine + para-aminobanzoic acid(PABA) + glutamic acid
Yellow crystals
Insoluble in water but its sodium salt is soluble in water
HAEMATINICS (FOLIC ACID)
28
29. Dietary sources : green leafy veg, egg, meat, milk
Daily requirement : 0.2 mg/day, during pregnancy and any condition
of high metabolic activity – 0.8 mg/day
HAEMATINICS (UTILLIZATION OF FOLIC ACID)
Present as Poly-glutamates
Additional glutamate residue
split off in upper intestine
before absorption
o Reduction to DHFA and methylation occurs at this site
o Absorption occurs by specific carrier mediated active transport in
intestinal mucosa
o Excreted by bile and urine
o Stored in hepatocytes
29
32. Glycoprotein hormone produced in juxtaglomerular cells of
kidney
Two forms – epoetin alpha and eportin beta
Uses –
Anaemia in chronic renal failure
Anaemia during chemotherapy of cancer, AIDS
To prevent anaemia in premature infants
To increase yield of blood before blood donation
32
HAEMATINICS (ERYTHROPOIETIN)
34. Coagulation, also known as clotting, is the process
by which blood changes from a liquid to a gel,
forming a blood clot.
Balance between pro-coagulants and anti-
coagulants
34
COAGULATION
35. 35
Category
Definition
Function
Importance
Examples
Pro-coagulants
It plays a key role in
blood coagulation
It facilitates blood
coagulation
Useful in sealing
severe injuries before
leading to complication
Thrombin and factor
Xa
Anti-coagulants
It has a key role to
prevent blood
coagulation
It blocks blood
coagulation
Blood thinning
medicines that
prevents formation
of blood clot in
patient with higher risk
of heart attack
Warfarin ,
Rivaroxaban,
Dabigatran, Apixaban
PRO-COAGULANTS AND ANTI-COAGULANTS
37. Blood flows in blood vessels will form a clot under
such conditions :
1) Trauma to vascular wall
2) Trauma to blood
3) Contact of blood with damages endothelial drugs
Process of coagulation is divided into 3 main steps
:
1) Formation of Prothrombin activator
2) Conversion of Prothrombin to Thrombin
3) Conversion of Fibrinogen to Fibrin
37
COAGULANTS (FACTORS)
38. 38
COAGULANTS (CASCADE OF BLOOD CLOTTING)
Formation of Prothrombin activator
Trauma to
blood or
contact of
Electro –VE
surface(glass)
Trauma to
vascular wall
or tissue
outside the
blood vessel
Prothrombin activator
