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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.
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.
• 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.
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.

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Blood products QN.pdf

  • 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.