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1. Anticoagulants.pptx
- 1. Yenepoya Pharmacy College& Research Centre Yenepoya (Deemed to be University), Deralakatte, Mangaluru Tahreen Taj Assistant Professor YPCRC
- 3. Specific Learning Objectives •At theend of the session, student should be able to • Define haemostasis • define and classify anticoagulants • Explain mechanism of action and pharmacology of Heparin and warfarin
- 4. Coagulants Haemostatcis /Coagulants :promotes coagulation & controls bleeding Types: 1. Local/styptic 2. Systematically • Other Methods : Physical Pressure, Ice
- 5. • Eg –Adrenaline, Thrombin, Fibrin. – Used locally – Local Haemostatcis called as Styptics – Styptics used on bleeding sites like tooth socket & wounds. (Adrenaline) • Eg – Vit K (fat soluble) – Essential for biosynthesis of clotting factor – Used systemically
- 7. Anticoagulants • These arethe drugs used to reduce the coagulability of blood OR It reduces fibrin formation MOA – By decrease action of coagulation factors – By interfering synthesis of factors
- 8.
- 9. Heparin • Heparin isa non-uniform mixture of straight chain mucopolysaccharides (10,000 – 20,000 kDa) • It contains polymers of two sulphated disaccharide units D-glucosamine- L-iduronic acid D-glucosamine – D- glucuronic acid
- 10. Characteristics • Discovery –1916 • Extracted from liver • Contains strong electronegative charges • Strong anticoagulant – act by in-vivo & in-vitro • Present in endoplasmic reticulum of mast cells • Richly present in Iung, liver and intestinal mucosa
- 11. Mechanism of actionof Heparin
- 12. MOA 1. Antithrombin IIIis synthesized in liver & circulates in plasma. 2. Heparin activates Antithrombin III – InhibitS the activated thrombin & Coagulation Factors Xa IXa –This is Physiological reaction. 3. Heparin Activates it by 1000 times = clotting time prolonged 4. Heparin & Antithrombin III inhibit activated factor X & Thrombin
- 13. Pharmacokinetics • As itis large molecule, it is not absorbed orally • Given by SC or IV Route • Should not be given as IM – Causes Haematos • Does not cross BBB and placenta, hence drug of choice during pregnancy • Metabolized in liver by heparinase • Excreted in urine
- 14. It should notbe given with • Penicillin • Tetracyclines • Hydrocortisone • Noradrenline in the same syringe or infusion bottle.
- 15. Adverse effects • Bleedingdue to over dose • Haematuria • Thrombocytopenia • Transient and reversible alopecia • Osteoporosis • Hypersensitivity reactions
- 16. Contraindications • Bleeding disorders •Severe hypertension • Threatened abortion, piles, g.i. ulcers • Subacute bacterial endocarditis • Ocular and neurosurgery • Chronic alcoholics, cirrhosis, renal failure • Aspirin and other antiplatelet drugs
- 17.
- 18. Warfarin • Discovery =1951 • They are antagonists of Vit-K • Reduces the plasma levels of functional clotting factors • Warfarin reduces the total amount of each vitamin K – dependent coagulation factors by 30–50%
- 19. Warfarin Action • Warfarinand its congeners act as anticoagulants only in vivo, not in vitro. Because they act indirectly by interfering with the synthesis Vit K dependent clotting factors VII, IX, X in liver. • They block gamma carboxylation of glutamate residue in = prothrombin VII, IX, X (necessary for clotting) • Action of Warfarin depends on the half life of clotting factors – Factor II - 60 hr – Factor VII- 6 hr – Factor IX – 24 hr – Factor X – 40 hr
- 20. Warfarin Action • Thoughthe synthesis of clotting factors diminishes within 2-4 hours of warfarin administration, anticoagulant effect develops slowly over the next 1- 3 days as levels of the clotting factors already present in plasma decline progressively. • Thus, there is always a delay between administration of the drug and the anticoagulant effect. Larger initial doses hasten the effect only slightly.
- 21. MOA No clotting Prevent coagulation Clottingfactor deficiency Incomplete coagulation factor molecule formed Blocks - Gamma carboxylation of glutamate residue in factor II, VII, IX, X
- 22. Descarboxy Factor II,VII, IXand X Factor II,VII, IX and X CO2, O2 γ-carboxylation by γ-Glutamyl carboxylase Vitamin Epoxide Reduced Vitamin K Warfarin NADH NAD+ Mechanism of action of Warfarin * Warfarin has no activity on fully carboxylated coagulation factors Calcium binding property Coagulation
- 23. Pharmacokinetics • Warfarin (COUMARIN)is 5 mg/day for 2–4 days, followed by 2– 10 mg/day • Completely absorbed in oral, i.v and rectal route • Almost bound to plasma proteins mainly to albumin • It is metabolized by Cytochrome P 450 enzymes CYP2C9 and CYP1A2. • Excreted in urine and stool • t 1/2 is 25 to 60 hours.
- 24. Warfarin • Contraindications • Bleedingdisorders • Severe hypertension • Threatened abortion, piles, • g.i. ulcers • Subacute bacterial endocarditis • Ocular and neurosurgery • Chronic alcoholics, cirrhosis, renal failure • Aspirin and other antiplatelet drugs Adverse effects • Bleeding • Alopecia • Dermatitis • Diarrhoea
- 25. anticoagulan • Antibiotics • Newercephalosporins • Aspirin • Drugs displacing protein binding: Suphonamides, phenytoin, probencid • Drugs inhibiting metabolism: chloramphenicol, cimetidine, tolbutamol and phenytoin • Liq. Paraffin: reduces Vit K absorption Decrease anticoagulant effect • Barbiturates • Oral contraceptive pills Drug interacions
- 26. • Deep veinthrombosis • Pulmonary embolism • Myocardial infarction • Unstable angina • Atrial fibrillation • Cerebrovascular diseases • Vascular surgery Uses of Anticoagulants
- 27.