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Anti Coagulants
Presented by:-
Shaikh Nisar Ali (M.Pharm)
Dept. Of Pharmacology
HKE’S matoshree Taradevi Rampure Institute of
Pharmaceutical Sciences.
Under the Guidance of:- Dr. Ashok K. Dastapur.
Anti Coagulants
• Anticoagulants, commonly known as blood thinners, are chemical
substances that prevent or reduce coagulation of blood, prolonging the clotting
time.
• As a class of medications, anticoagulants are used in therapy for thrombotic
disorders.
• Oral anticoagulants (OACs) are taken by many people in pill or tablet form, and
various intravenous anticoagulant dosage forms are used in hospitals.
• Some anticoagulants are used in medical equipment, such as sample tubes, blood
transfusion bags, heart-lung machines, and dialysis equipment.
Classification of Anti-Coagulants.
In Vitro Anticoagulants: -
• These compounds are chelating agents like citrates , fluorides
and ED.T.A. ( Ethylene diamine tetra acetic acid ) .
• They act by removing calcium ions . These compounds are used
in vitro to preserve blood ( so as to make it suitable for
transfusion ).
In Vivo anticoagulants.
( Slow acting anticoagulant)
COUMARIN DERIVATIVES : -
Dicoumarol
Cyclocoumarol
Phenprocouman
Ethyl Biscoumacetate
DICOUMAROL( Bishydroxycoumarin) :-
• Dicoumarol was carlier isolated from spoilt sweet clover hay. In
cattle, it produced sweet clover disease which is characterised
by severe bleeding.
• It is effective orally.
MECHANISM OF ACTION: -
• Dicoumarol acts by inhibiting the synthesis of prothrombin and
factors VII, IX and X in the liver.
• For the synthesis of prothrombin. vitamin K is necessary.
Dicoumarol acts as a compctitive antagonist of vitamin K.
• The anticougulant effect of dicoumarol is antagonised by
vitamin K.
Anticoagulants Drugs.
ABSORPTION , FATE AND EXCREATION: -
• Dicoumarol is effective on oral and intravenous administration.
• In blood, it is bound to albumin. High concentration is present in
liver. It crosses placental barrier and also is secreted in milk.
• It is eliminated in urine, mostly in a metabolised form.
ADVERSE REACTION: -
• Haemorrhage is the major toxicity.
• This may occur as haematuria, bloody stools, bleeding of gums etc.
• These effects can be treated by large doses of vitanmin K.
DOSE: -
300 mg on first day. 200mg on second day. And 50-100 mg on
subsequent days by oral route,
Indanediones: -
1. Pheninione
2. Diphenadione
3. Anisindione
4. Chlorphenindione
• The indanediones are effective on oral and parenteral administration.
They act by inhibiting prothrombin synthesis like dicoumarol.
• They have a rapid onset and short duration of action.
• Toxicities of indanediones are haemorrhage, hepatitis and skin reactions.
Warfarin: -
• It was orginally used as a rat poison.
• It is well soluble and so can be administered by all routes.
• It act by the same mechanism as dicoumarol.
• It has a bronchodilator and coronary vasodilator effect.
• Haemorrhage is the important toxicity and it can by controlled
by vitamin K.
• Other toxicities are alopecia, urticaria and dermatitis.
Both In vitro and In vivo Anticoagulants.
(Fast Acting Anticoagulants)
HEPARIN:
SOURCE: -
• Heparin was first extracted from liver. It is also obtained from lungs
and intestinal mucosa.
• In these tissues, it is present in mast cells. Heparin is released from
mast cells during anaphylactic shock.
Heparin is a highly negative charged mucopolysaccharide that is
prepared commercially from bovine lung and Porcine intestinal
mucosa.
Because of its highly negatively charge and large molecular size it is
administered parenterally.
MECHANISM OF ACTION: -
• Heparin prevents clotting both in vivo and in vitro. It does not inhibit
prothrombin synthesis. It acts by the following mechanisms :
• 1. It binds to antithrombin Il (heparin co - factor). This combination inactivates
serum coagulation factors.
• 2. It inhibits factor Xa mediated conversion of prothrombin to thrombin.
• 3. It also inhibits thrombin (Ila) mediated conversion of fibrinogen to fibrin.
PHARMACOLOGICAL ACTIONS: -
• These prolong the clotting time of blood in both Vivo and vitro .
• Injected heparin causes the release of tissue bound lipoprotein lipase which
hydrolyse the triglycerides of Chylomicrons and LDL bound to capillary
endothelial cells.
• Heparin suppresses the rate of aldosterone secretion and also the concentration
of free tyroxine .
Cont. .
• Heparin slows wound healing and also depresses cell mediated
immunity.
• Heparin is higher doses inhibits platelet aggregation prolonged
bleeding.
ABSORPTION, FATE AND EXCREATION: -
• Heparin is ineffective orally. It is well absorbed after subcutaneous
injection. On intravenous injection, it produces immediate
anticoagulant effect.
• Heparin should not be used intramuscularly because it produces
hematoma.
• Heparin does not cross placental barrier. Also it is not secreted in
milk. It is metabolised in the liver by an enzyme called heparinase.
It is eliminated in urine both in an inactive and as a metabolised
form.
ADVERSE REACTION: -
• Danger of bleeding due to over dosage.
• Allergic and anaphylactic reactions.
• Alopecia on prolonged use.
PREPARATION AND DOSAGE: -
• Heparin is available as sodium or calcium heparin.
• I.V bolus -5000 to 10000 units every 4 to 6 hours.
• Subcutaneous injections-25000 units every 12-24 hours.
Thank you

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Anticoagulants Drugs.

  • 1. Anti Coagulants Presented by:- Shaikh Nisar Ali (M.Pharm) Dept. Of Pharmacology HKE’S matoshree Taradevi Rampure Institute of Pharmaceutical Sciences. Under the Guidance of:- Dr. Ashok K. Dastapur.
  • 2. Anti Coagulants • Anticoagulants, commonly known as blood thinners, are chemical substances that prevent or reduce coagulation of blood, prolonging the clotting time. • As a class of medications, anticoagulants are used in therapy for thrombotic disorders. • Oral anticoagulants (OACs) are taken by many people in pill or tablet form, and various intravenous anticoagulant dosage forms are used in hospitals. • Some anticoagulants are used in medical equipment, such as sample tubes, blood transfusion bags, heart-lung machines, and dialysis equipment.
  • 4. In Vitro Anticoagulants: - • These compounds are chelating agents like citrates , fluorides and ED.T.A. ( Ethylene diamine tetra acetic acid ) . • They act by removing calcium ions . These compounds are used in vitro to preserve blood ( so as to make it suitable for transfusion ).
  • 5. In Vivo anticoagulants. ( Slow acting anticoagulant) COUMARIN DERIVATIVES : - Dicoumarol Cyclocoumarol Phenprocouman Ethyl Biscoumacetate
  • 6. DICOUMAROL( Bishydroxycoumarin) :- • Dicoumarol was carlier isolated from spoilt sweet clover hay. In cattle, it produced sweet clover disease which is characterised by severe bleeding. • It is effective orally. MECHANISM OF ACTION: - • Dicoumarol acts by inhibiting the synthesis of prothrombin and factors VII, IX and X in the liver. • For the synthesis of prothrombin. vitamin K is necessary. Dicoumarol acts as a compctitive antagonist of vitamin K. • The anticougulant effect of dicoumarol is antagonised by vitamin K.
  • 8. ABSORPTION , FATE AND EXCREATION: - • Dicoumarol is effective on oral and intravenous administration. • In blood, it is bound to albumin. High concentration is present in liver. It crosses placental barrier and also is secreted in milk. • It is eliminated in urine, mostly in a metabolised form. ADVERSE REACTION: - • Haemorrhage is the major toxicity. • This may occur as haematuria, bloody stools, bleeding of gums etc. • These effects can be treated by large doses of vitanmin K. DOSE: - 300 mg on first day. 200mg on second day. And 50-100 mg on subsequent days by oral route,
  • 9. Indanediones: - 1. Pheninione 2. Diphenadione 3. Anisindione 4. Chlorphenindione • The indanediones are effective on oral and parenteral administration. They act by inhibiting prothrombin synthesis like dicoumarol. • They have a rapid onset and short duration of action. • Toxicities of indanediones are haemorrhage, hepatitis and skin reactions.
  • 10. Warfarin: - • It was orginally used as a rat poison. • It is well soluble and so can be administered by all routes. • It act by the same mechanism as dicoumarol. • It has a bronchodilator and coronary vasodilator effect. • Haemorrhage is the important toxicity and it can by controlled by vitamin K. • Other toxicities are alopecia, urticaria and dermatitis.
  • 11. Both In vitro and In vivo Anticoagulants. (Fast Acting Anticoagulants) HEPARIN: SOURCE: - • Heparin was first extracted from liver. It is also obtained from lungs and intestinal mucosa. • In these tissues, it is present in mast cells. Heparin is released from mast cells during anaphylactic shock. Heparin is a highly negative charged mucopolysaccharide that is prepared commercially from bovine lung and Porcine intestinal mucosa. Because of its highly negatively charge and large molecular size it is administered parenterally.
  • 12. MECHANISM OF ACTION: - • Heparin prevents clotting both in vivo and in vitro. It does not inhibit prothrombin synthesis. It acts by the following mechanisms : • 1. It binds to antithrombin Il (heparin co - factor). This combination inactivates serum coagulation factors. • 2. It inhibits factor Xa mediated conversion of prothrombin to thrombin. • 3. It also inhibits thrombin (Ila) mediated conversion of fibrinogen to fibrin. PHARMACOLOGICAL ACTIONS: - • These prolong the clotting time of blood in both Vivo and vitro . • Injected heparin causes the release of tissue bound lipoprotein lipase which hydrolyse the triglycerides of Chylomicrons and LDL bound to capillary endothelial cells. • Heparin suppresses the rate of aldosterone secretion and also the concentration of free tyroxine . Cont. .
  • 13. • Heparin slows wound healing and also depresses cell mediated immunity. • Heparin is higher doses inhibits platelet aggregation prolonged bleeding. ABSORPTION, FATE AND EXCREATION: - • Heparin is ineffective orally. It is well absorbed after subcutaneous injection. On intravenous injection, it produces immediate anticoagulant effect. • Heparin should not be used intramuscularly because it produces hematoma. • Heparin does not cross placental barrier. Also it is not secreted in milk. It is metabolised in the liver by an enzyme called heparinase. It is eliminated in urine both in an inactive and as a metabolised form.
  • 14. ADVERSE REACTION: - • Danger of bleeding due to over dosage. • Allergic and anaphylactic reactions. • Alopecia on prolonged use. PREPARATION AND DOSAGE: - • Heparin is available as sodium or calcium heparin. • I.V bolus -5000 to 10000 units every 4 to 6 hours. • Subcutaneous injections-25000 units every 12-24 hours.