This document summarizes drugs that affect the blood, including cyanocobalamin, ferrous sulfate, folic acid, adrenochrome, mono semicarbazone, heparin sodium, and vitamin K. It describes the mode of action, pharmacokinetics, indications, dosages, administration routes, adverse effects, interactions, and toxicity of these drugs. The drugs covered work by various mechanisms including increasing red blood cell production, inhibiting blood clotting, and facilitating blood clotting factor synthesis. Their use spans treating anemias, hemorrhage, coagulation disorders, and as anticoagulants. Close monitoring of patients is often required when using these drugs.

1. DRUGS AFFECTING THE BLOOD
Drugs CYANOCOBALAMINE FERROUS SULPHATE
FOLIC ACID TABLETS
ADRENOCHROME
MONOSEMICARBA
ZONE
Inj. Heparin Sodium Vitamin K
Description water-soluble, found in
liver, meat and eggs,
daily requirements of 3 –
5 mcg, no plant source
Sulphate salt of iron -60 mg of
elemental iron. Folic acid is a
water-soluble vitamin and tablet
contains 5 mg.
oxidation product
of
adrenaline.Tablet
adrenochrome also
contains vitamin K.
vitamin C and
calcium phosphate.
heterogeneous group of anionic
mucopolysaccharides called
glycosaminoglycans
having anticoagulant properties.
Derived from porcine intestinal
mucosa.
fat-soluble vitamin which is
necessary for the synthesis of
clotting factors II, VII, IX, X. It
is found in green leafy
vegetables as vitamin
K1(phytomenadione,dosage
form).also synthesized by
intestinal flora (K2 –
menaquinone).
Mode of
Action
exists in the body as
methyl cobalamine and
its derivatives,
coenzymes in
carbohydrate and lipid
metabolism, purine
and pyrimidine synthesis
and thereby DNA
synthesis, Deficiency,
decrease in RBC
production and hence
anaemia
Iron -component of Hb. present in
small amounts in myoglobin,
enzymes(cytochromes, catalase)
and in Iron deficiency ineffective
erythropoiesis > reduction of RBC
production > reduced tissue
oxygen Delivery.
Folic acid exists in the body as
dihydrofolate and
tetrahydrofolate > amino acid
metabolism and purine synthesis.
Deficiency> decreased nucleotide
and DNA synthesis> maturation
arrest in RBCs and deficiency
states.
haemostatic –
controls bleeding
and oozing from
raw surfaces by
reducing capillary
fragility, thereby it
prevents bleeding
from the
microvasculature.
inhibits the reactions that lead to
the clotting of blood by acting
multiple sites in the
coagulation cascade. It combines
with anti-thrombin III and prevents
conversion of
prothrombin to thrombin. If
thrombosis has already occurred, it
inhibits further extension of
the clot and also prevents
stabilization of the formed clot.
Vitamin K is an essential
cofactor for the enzyme
which converts the
precursors of clotting
factors II, VII, IX, X into their
active forms.
PK Absorbed orally Fe2+
and
transported to the liver as
transferrin. Storage form-ferrtin.
Bone marrow and reticulo
endothelial system formation of
haem and is incorporated in RBCs
as haemoglobin. Excess is lost in
the feaces.
Folic acid is well absorbed from
the GIT and excess is excreted in
the urine.
Following subcutaneous injections,
peak levels are obtained 4 hours
after administration. It is
extensively bound to plasma
proteins. Heparin is taken up by the
reticulo endothelial system
and liver and degraded.
readily absorbed on IM
administration and
concentrated in the liver. It
has no effect in
ordinary individuals, but in
those with vitamin K
deficient haemorrhagic
states, action is seen in 3 – 6
hours and prothrombin levels
are normal in 12 –14 hours.

2. Indication megaloblastic anemia in
pregnancy and lactation,
malabsorption
syndromes, gastric and
intestinal surgery in
states where B12
requirements are
increased –
thyrotoxicosis
haemorrhage or
malignancy.
Prophylactic use- pregnancy and
lactation, menstruating women,
infants, children and long-term
therapy with NSAIDS.
•Iron deficiency anaemia –
malnutrition, patientseith
gastrectomy, malabsorption
syndrome.
• Folic acid > folate deficiency,
patients on anti-epileptics and for
prevention of neural tube defects
in the fetus during pregnancy.
•Epistaxis.
• Haematuria.
•Secondaryhaemor
rhage from
wounds.
• Retinal
haemorrhage. •
Menorrhagia,Metr
orrhagia.
• Prior to surgery
to reduce bleeding.
• Anticoagulant therapy in
prophylaxis of deep vein thrombosis
• Prevention of reocclusion after
thromobolysis in mgt of MI
and acute arterial occlusion.
• Prevention of extension of already
existing deep vein thrombosis.
• pulmonary embolism
• Atrial fibrillation with
thromboembolic phenomenon.
• Disseminated intravascular
coagulopathy.
• Prevention of clotting in arterial or
heart surgery.
• Anticoagulant used in blood
transfusions or dialysis procedures
or extracorporeal
circulations.
• Prevention of clotting of blood
samples in laboratories.
Bleeding disorders due to
faulty formation of
prothrombin, VII, IX, X
because of vitamin
deficiency or interference
with its action like:
• Oral anticoagulant induced
prothrombin deficiency.
• Haemorrhagic disease of
newborn – prophylaxis and
therapy.
• Hypoprothrombinemia due
to defective absorption of
vitamin K
•obstructive jaundice, biliary
fistula, sprue, ulcerative
colitis, cardiac disease,
intestinal resection, ileal
bypass, cystic fibrosis.
Dosage Treatment of deficiency:
100 mcg of B12 /day for
2 weeks; then 100 mcg
per month as
maintenance dose.
For prophylaxis: 100
mcg/month.
R/A I.M. Oral • Oral – most
effective.
• Parenteral – I.M.
Injection.
• IV infusion,
• SC,
• IM,
• SC
Contraind. •patients with
hypersensitivity
• Patients with haemolytic
anaemias, haemochromatosis,
haemosiderosis.
• Intolerance to oral iron
preparations.
Hypersensitivity • Thrombocytopenia.
• When lab facilities for monitoring
of TT/APTT are not available.
• Bleeding condition like active
peptic ulcer, esophageal varices,
piles etc, and blood dyscrasias.
• Uncontrolled hypertension,
bacterial endocarditis.
• Recent surgery or trauma.
History of hypersensitivity or
anaphylactic reactions to
previously administrated
dose of vitamin K.

3. • Menstruation.
• Hypersensitivity to heparin.
• Intracranial haemorrhage.
• Proliferative retinopathy.
• Severe liver disease and renal
failure.
Precaution
s
• Response to treatment
(increase in RBC count)3-
4 weeks
•Periodic monitoring of
reticulocyte and RBC
count is necessary.
•along with folic acid
(5mg) for the treatment
of megaloblasitc anemia.
•Do not mix with vitamin
K, dextrose,
chlorpromazine or other
oxidizing or reducing
agents in the same syring
• improvement of RBC counts 3-4
weeks after initiation of therapy.
• Response to therapy> monitored
by periodic reticulocyte and red
blood cell counts.
vitamin C enhances iron
absorption.
• Duration of treatment depends
on the rate of recovery and the
amount of blood loss. If a
positive balance can be created
with adequate iron stores,
withdrawal of therapy can be
done.
• Administration Instruction:
Administer along with food for
decreasing gastro intestinal
effects.
Use with caution in
children. Patients
over 60, pregnancy
and in lactation.
• Adjust dosage so that the bleeding
time is 2.5 - 3 times the normal
value monitors the patient by APTT
time.
• Always monitor patient for signs of
haemorrhage – unexplained
hypotension, pallor etc.
• Platelet count should be
monitored in patients receiving
heparin for more than a few days
since it has caused
thrombocytopenia with severe
thromboembolic complications. It
should be discontinued if
thrombocytopenia develops.
• Dosage reduced in elderly people.
• Administration instructions:
- For making up I.V. infusion, use
normal saline as diluent.
- Heparin should not be given by IM.
- Aminoglycosides are incompatible
with heparin and should not be
given in the same cannula.
• Prothrombin levels will rise
only after 1 – 3 hours of
administration of vitamin K
and effects should not be
expected immediately.
• Cannot be used for
bleeding induced by heparin.
• Regular monitoring of
prothrombin levels to check
for therapeutic action.
• Should be administrated
with caution in premature
infants-haemolysis and
jaundice can occur.
•Administration
instructions:
- IV route not recommended
as it can cause dyspnoea,
chest pain, etc., if
unavoidable, administer very
slowly, rate not more than 1
mg/min.
Adverse
effct.
allergic reactions may
occur like dyspnoea,
bronchospasm, skin
reaction etc.,
• Nausea, abdominal pain, G.I.
distress, constipation
• Black discoloration of stools.
Rare effects:
• Hypersensitivity reactions
Common effects:
• Haemorrhage – can be minor
(bleeding from venepuncture sites)
or major (internal bleeds).
• Thrombocytopenia – due to
platelet aggregation induced by
heparin.
• Local irritation – pain, erythema,
ulceration.
Pain at the site of injection
may occur.

4. Rare effects:
• Hypersensitivity – chills, fever,
urticaria, anaphylactoid reactions
may occur.
• Following Long-term use –
osteoporosis, SGOT and SGPT
elevation can occur.
• Skin necrosis.
Toxicity Toxic dose is 2 – 10 gm.
Acute abdominal pain, bloody
diarrhoea, vomiting of brown or
bloody stomach contents,
pallor, cyanosis, drowsiness,
stupor, coma, CVS collapse and
metabolic acidosis
Continuous infusion has led to
serious complications (hemorrhage)
and acute
thrombocytopenia, leading to shock
and death.
Facial flushing, sweating,
chest constriction, chest pain,
dyspnoea, cyanosis and CVS
collapse have been reported
following rapid I.V. infusion
of vitamin K.
Treatment
of toxicity
•Emesis, lavage with bicarbonate,
phosphate compounds to
precipitate unabsorbed iron.
•Desferrioxamine for
neutralization of systemically
absorbed iron.
• Monitor ECG, Vital signs, fluid
and electrolyte balance.
• Slow intravenous infusion of
protamine sulphate (calculate the
dose of protamine sulphate to be
given by the principle: 1 mg of
protamine sulphate neutralizes 100
units of heparin).
• Not more than 50 mg of
protamine sulphate to be injected
per dose. Alternatively, give fresh
blood or plasma or clotting factors.
Supportive and symptomatic.
Drug
Interaction
Non – fatal:
• Iron reduces the absorption of
tetracycline’s, quinolones and
penicillamine.
• Drugs reducing iron absorption –
antacids, eggs and milk.
• Response to iron therapy may
be delayed in patients taking
chloramphenicol.
Antihistamines
reduce the efficacy
of the drug.
Vitamin K status may be
altered in warfarin therapy.