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ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE
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ANTI-HEMOSTATIC DRUGS IN VETERINARY PRACTICE

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BRIEF note on classification of various anticoagulants, thrombolytics & antiplatelet drugs along with indications and doses.

BRIEF note on classification of various anticoagulants, thrombolytics & antiplatelet drugs along with indications and doses.

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  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
  • September 2007
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  • Transcript

    • 1. ANTIHAEMOSTATICS ASSIGNMENT PRESENTED TO DR SUJITH S ASST PROFESSOR , DEPT OF VPT , COVAS , POOKODE PRESENTED BY DR SINDHU K MVSc SCHOLAR
    • 2. AGENTS WHICH REDUCES HEMOSTASIS / BLOOD CLOTTING 1) ANTICOAGULANTS In vitro & systemic 2) THROMBOLYTICS Plasminogen activators 3) ANTIPLATELET DRUGS COX inhibitors , glycoprotein IIa/IIIb inhibitors , thromboxane inhibitors & ADP inhibitors
    • 3. Components of hemostatic System:- 1) Platelets 2) Plasma proteins – Coagulation & Fibrinolytic factors & inhibitors 3) Vessel wall itself(endothelium) Steps of normal homeostasis :- 1} platelet plug formation • Adhesion, activation, aggregation 2}Fibrin clot formation • Coagulation - intrinsic - extrinsic 3}Dissociation of clot
    • 4. Vascular Injury Exposure of collagen and vWF Tissue factor exposure Platelet adhesion and release Activation of coagulation Platelet recruitment and activation Thrombin generation Fibrin formationPlatelet aggregation Platelet – fibrin thrombus
    • 5. ANTI COAGULANTS 1] In vitro use To prevent clotting of blood for transfusion or diagnostic use 2] In vivo use To prevent development & enlargement of thrombi
    • 6. IN-VITRO ANTICOAGULANTS • For lab purposes – sodium oxalates , sodium fluoride , EDTA • For blood transfusion – ACD solution , CPDA-1 solution
    • 7. OXALATES 1} sodium oxalate – combines with blood calcium forming insoluble calcium oxalate rendering calcium unavailable for blood coagulation Dose – conc of 20 % @ level of blood 0.01 ml / 1 ml blood ( 2mg/ml) ALL OXALATE SALTS ARE TOXIC Contraindicated – blood transfusion -- systemic use
    • 8. SODIUM FLUORIDE • Excellent anticoagulant for blood glucose studies bcoz it interferes with enzymes involved in glycolysis • It acts as preservative • Dose 2.5 mg / ml of blood for blood glucose preservation
    • 9. ETHYLENE DIAMINE TETRA ACETIC ACID • EDTA ( edetate disodium , USP ) MOA – Na & K salts of EDTA chelates blood calcium thus preventing clotting • Lab application 1} hematological count { thrombocyte count } bcoz Cellular details preserved Dose – 1 mg / 5 ml of blood 0.01 ml of 2 % EDTA solution / ml of blood
    • 10. BLOOD TRANSFUSION 1] Acid Citrate Dextrose , USP Sodium citrate – 25 g Citric acid – 8 g Dextrose – 24.5 g Distilled water to make volume of 1000 ml Dose – at level of 15 ml / 100 ml of blood Toxicity in dogs should not cross 286mg/kg
    • 11. ` 2] Citric Phosphate Dextrose Adenine CPDA-1 In DOGS maintains high levels of erythrocyte post transfusion viability up to 20 days 3] Heparin In cats - To collect small quantity of blood ( 50 ml )for transfusion Lab purpose : 8 – 10 units of heparin / ml of blood Blood transfusion : 4 – 6 units of heparin / ml of blood
    • 12. SYSTEMIC ANTICOAGULANTS 1} Heparin & related compounds 2} Inhibitors of vitamin K 3} Direct inhibitors of coagulation factors 4} Miscellaneous anticoagulants
    • 13. HEPARIN ( HEPARIN SODIUM , USP ) • Pharmaceutical graded heparin is prepared from bovine lung tissue or porcine intestinal mucosa • It is a heterogenous mixture of anionic sulfated mucopolysaccharide with molecular weight ranging from 1200 – 40000 daltons. • Sodium salts used in vivo. • Calcium salts , potassium salts – therapeutic use.
    • 14. MOA • Anti coagulatory effect of heparin – the reversible binding of heparin to AT III , a protease inhibitor & Heparin Co factor II • Binded heparin accelerates the velocity of interaction between coagulant inhibitory factors & clotting factors • LMWH – inactivates only factor Xa • HMWH – inactivates thrombin & blocks conversion of fibrinogen to fibrin , neutralizes activated factor IX
    • 15. P K & P D • Administered dose of heparin bounds extensively: endothelial cells macrophages plasma proteins Stored pools ~> saturated ~> free heparins ~>plasma ~> excretion kidney Metabolism – liver - Reticulo endothelial system
    • 16. CLINICAL INDICATION • Prevention / treatment of venous thrombosis ( red thrombus ) • Pulmonary embolism • Management of DIC • Arterial fibrillation with embolization Eg: feline cardiomyopathy • Other potential coagulable states Eg: cushing`s disease nephrotic syndrome cardiomyopathy
    • 17. GUIDE LINE FOR HEPARIN DOSAGE 1} High dose heparin therapy Aims to increase APTT 1.5 – 2.5 times base line & ACT 1.2 – 1.4 times base line Initial high loading dose is beneficial Regular & frequent monitoring of clotting time s essential Clinical indication – treatment of established THROMBOEMBOLI Dogs : 150 – 250 U / kg TID Cats : 250 – 375 U / kg TID
    • 18. 2} LOW DOSE HEPARIN THERAPY Dogs : treatment & management of Heart worm infestation Initial dose 100 – 200 U / kg i/v followed by 50 U / kg every 3 hours Maintenance dose 40 – 80 U / kg TID s/c Cats : treatment of feline cardiomyopathy 200 U / kg s/c TID Horses : management of DIC high grade DIC : 80 – 100 U / kg i/v after 4-5 hr repetation low grade DIC : 25 – 40 U / kg s/c BID / TID daily
    • 19. MANAGEMENT OF DIC ~ DISSEMINATED INTRAVASCULAR COAGULOPATHY Heparin + blood / plasma Low dose regimen for management Small animals : 75 U / kg TID Horses : 25 – 100 U / kg TID Effect on APTT = minimum
    • 20. LOW MOLECULAR WEIGHT HEPARINS • Are short chain of polysaccharide with molecular weight of 1000- 10000 Da • Isolated from standard heparin by techniques - Gel filtration chromatography - differential precipitations with ethanol Advantages: better absorption from s/c injection : prolonged elimination half life : lower incidences of hemorrhagic complications
    • 21. MOA • LMWH selectively inhibit factor Xa with little effect on thrombin , Factor II ~> result is little effect on APTT & whole blood clotting time • LMWH less anti platelet action • Commercial preparations – Ardeparin , Bemiparin , Dalteparin , Enoxaparin , Reviparin , Nadroparin , Tinzaparin
    • 22. HEPARINOIDS • Non heparin naturally occurring & synthetic sulphated glycosaminoglycans which posses heparin like anticoagulant action 1} DANAPAROID (Orgaron*) Mixture of non heparin glycosamines isolated from porcine intestinal mucosa Orgaron* consists ~ heparin sulphate 80 % ~ dermatan sulphate 8 -16 % ~ chondroitin sulphate < 8.5 %
    • 23. MOA • Acts mainly by enhancing the inhibition of factor Xa by antithrombine • Danaproid exerts a strong catalytic effects on the inactivation of factor Xa than on the inactivation of thrombin Clinical indications • Prevention of DEEP VEIN THROMBOSIS ( DVT ) following orthopaedic , major abdominal & thoracic surgery • Patients with positive diagnosis of non hemorrhagic stroke
    • 24. OTHER DRUGS 1] drotrecogin alfa 2] dextran sulphate 3] sulodexide
    • 25. VITAMIN K ANTAGONISTS • Inhibitors of vitamin K often called as ORAL ANTICOAGULANTS • VIT K antagonists are active ORALLY (only IN VIVO ) • Studies in veterinary medicine focused primarily on their TOXIC effects rather than on therapeutic indications TYPES 1} Coumarin derivatives 2} Indanedione derivatives
    • 26. COUMARIN DERIVATIVES • Coumadins are synthetic oral anticoagulants derived from the molecule 4 hydroxycoumarin 1} BISHYDROXYCOUMARIN – first oral AC synthesized by LINK (1943-44) Its a derivative of moldy / spoiled sweet clover which is responsible for hemorrhagic disease in cattle in USA 2} WARFARIN SODIUM (USP) 2nd compound synthesized commercially
    • 27. WARFARIN: MOA • Inhibiton of hepatic synthesis of vit K dependent clotting factor ~ Prothrombin ~ Factor VII , IX , X ~ anticoagulant protein C & S Carboxylation results in the oxidative inactivation of vit K Warfarin inhibits vit K epoxide reductase enzyme & interfere with regeneration of active form of vit K thereby inhibiting synthesis of prothrombin & factor VII , IX , X
    • 28. ` • Warfarin acts as AC only IN VIVO bcoz they act indirectly by interfering with synthesis of clotting factors • AC effects develops over several hours but peak plasma level occurs in 1 hour after oral administration onset takes 6 -12 hours with full benefits realized after (2-3 days) & long duration of action (4-7 days) • bcoz of persistence of factors synthesized before drug administration & of long half life • Rapidly & completely absorbed from intestine • Metabolised in liver ~ inactive metabolites cytochrome P450 system
    • 29. ADVERSE EFFECTS • Acute internal bleeding/hemorrhage • Clinical signs ~ anaemia , thrombocytopenia , hematuria etc • Hemorrhages in brain & spinal column ~ ataxia , paresis , convulsions • Periarticular hemorrhages ~ lamness , joint swelling , pain LAB CONTROL 1} the quick test 2} the one stage prothrombin time
    • 30. CLINICAL INDICATIONS • Prophylaxis of venous thrombosis & Aortic/ pulmonary thromboembolism Horses : to relieve the clinical signs of NAVICULAR DISEASE Dose @ 0.02 mg/kg PO once daily Dogs : for prevention of recurrence of thrombotic conditions Dose @ 0.1 – 0.2 mg/kg PO once daily
    • 31. INDANEDIONE DERIVATIVES • Are derivative of indane-1,3-dione • Structurally related to coumarins & produce anticoagulation activity by mechanism involving ANTAGONISM OF VITAMIN K • Reports to cause kidney damage, sensitivity reactions, leucopenia in humans. Hence retricted drugs category • Use in vety practice not reported yet Eg: Anisindione , phenindione , clorindione , diphenadione
    • 32. DIRECT INHIBITORS OF COAGULATION FACTORS 1} Direct inhibitors of factor Xa – Xabans -- Rivaroxabans 2} Direct inhibitors of coagulation factor II – hirudin -- bivalirudin -- desirudin & lepirdin 3} Direct thrombin inhibitors – argatroban -- dabigatran
    • 33. END OF TOPIC - ANTICOAGULANTS DISCUSSIONS
    • 34. THROMBOLYTICS • Drugs that enhances the conversion of the inactive precursor plasminogen to the active fibrinolytic enzyme plasmin • 2 phases Plasminogen ~ plasma/soluble phase • ~ gel phase • Dissolves both physiologic as well as pathogenic thrombus = TOXIC ,producing hemorrhage = major side effect
    • 35. MOA • When plasminogen activating agents + clot = activation of fibrin bound gel phase plasminogen to plasmin locally with selective fibrinolysis • Instead soluble phase plasminogen circulating in systemic blood also activated • Adverse effect = increased tendency for systemic bleeding • Plasmin formation occurs through out circulation = overactivation of plasminogen , neutralizing endogenous antagonist to plasmin a2 ANTIPLASMIN
    • 36. THROMBOLYTIC DRUGS – MECHANISM OF ACTION
    • 37. THROMBOLYTIC DRUGS – MECHANISM OF ACTION
    • 38. THROMBOLYTIC DRUGS – MECHANISM OF ACTION
    • 39. THROMBOLYTIC DRUGS – MECHANISM OF ACTION
    • 40. FIRST GEN : STREPTOKINASE • Streptokinase is a protein obtained from group C BETA HEMOLYTIC STREPTOCOCCI • Effective & inexpensive clot dissolving drug ~ MI • ~ Pulmonary embolism • MOA :acts as plasminogen activator = enhances production of plasmin by forming an active non covalent 1:1 complex (streptokinase : plasminogen complex ) • Plasmin catalyzes degradation of plasma proteins = clotting factor FIBRINOGEN & factor V , VII
    • 41. ADVERSE EFFECT • Foreign protein = Antigenic reactions • 2nd time use = hypersensitivity & Anaphylaxis • Over dosage = plasminogen depletion & SK resistance • Treatment over-dosage FRESH PLASMA /AMINOCAPROIC ACID
    • 42. CLINICAL INDICATIONS • Used locally as powder , infusion or irrigation of wounds which don’t responds for antibacterial therapy – burns , ulcers , chronic eczema , ear hematomas , otitis externa , osteomyelitis , chronic sinusitis • Parentrally ~ eczema , dermatitis , hematoma , trauma & pneumonia • Prophylaxis ~ reduction of post operative adhesions • Dogs: 5000 – 10,000 U (total dose) IM IV in 2 divided doses 5 days • Large animals : 5000 – 10,000 U / 45 kg BW , IM IV 2 divided dose 5 – 6 days
    • 43. SEC GEN : PLASMINOGEN ACTIVATORS • Tissue plasminogen activators • Alteplase • Reteplase • Urokinase • Streptodornase OTHER DRUGS ~ ancrod ~ fibrinolysin
    • 44. MOA • It catalyzes conversion of plasminogen to plasmin • Selective action towards the plasminogen bound to fibrin & low affinity for free plasminogen • Thus fibrinolysis to the formed clot , with out unwanted degradation of other proteins Clinical indication 1} thromboembolic strokes 2} deep vein thrombosis 3} pulmonary embolism to clear a blocked artery
    • 45. • ALTEPLASE – treatment of aortic thromboembolism Cats : 0.25 – 1 mg/kg/hour , i/v infusion for total dose of 1-10 mg/kg Dogs : 0.01 microgram/kg/min , i/v infusion for 30 min • UROKINASE – to prevent post operative lesions Dogs : 5000 – 10,000 units/kg , intra-peritoneal lavage
    • 46. END OF TOPIC - THROMBOLYTICS DISCUSSIONS
    • 47. ANTITHROMBOTIC DRUGS
    • 48. ANTITHROMBOTIC DRUGS
    • 49. ANTITHROMBOTIC DRUGS
    • 50. ANTITHROMBOTIC DRUGS
    • 51. THE ROLE OF PLATELETS
    • 52. THE ROLE OF PLATELETS
    • 53. THE ROLE OF PLATELETS
    • 54. THE ROLE OF PLATELETS
    • 55. ANTITHROMBOTIC DRUGS Antiplatelet drugs Acetylsalicylic acid (aspirin) P2Y12 antagonists Dipyridamole GPIIb/IIIa antagonists Used widely in patients at risk of thromboembolic disease Beneficial in the treatment and prevention of ACS and the prevention of thromboembolic events Secondary prevention in patients following stroke, often in combination with aspirin Administered intravenously, are effective during percutaneous coronary intervention (PCI)
    • 56. COX INHIBITORS • Aspirin ~ NSAID • MOA = irreversibly inactivates cyclooxygenase enzyme to produce pharmacological effects Reduces synthesis of thromboxane A2 = potent vasoconstrictor & inducer of platelet aggregation • Irreversibly acetylate thromboxane synthase , enzyme responsible for thromboxane synthesis • Low dose = effective in reducing platelet aggregation • High dose = blocks synthesis of prostacyclin reducing over all anti aggregatory effect
    • 57. Plaque Disruption Collagen vWF Platelet adhesion and secretion Aspirin Thrombin generation Abciximab Eptifibatide Tirofiban Platelet aggregation Platelet recruitment and activation X COX-1 TXA2 ADP X GPllb / llla activation X
    • 58. CYCLOOXYGENASE INHIBITORS – MECHANISM OF ACTION
    • 59. ACETYLSALICYLIC ACID – MECHANISM OF ACTION
    • 60. ACETYLSALICYLIC ACID – MECHANISM OF ACTION
    • 61. ACETYLSALICYLIC ACID – MECHANISM OF ACTION
    • 62. ACETYLSALICYLIC ACID – MECHANISM OF ACTION
    • 63. GLYCOPROTEIN II B / III A INHIBITORS • NEW CLASES of potent platelet aggregation agonists • MOA – acts by blocking glycoprotein II b / III a receptors present on surface of platelets • Glycoprotein II b / III a complex functions as receptor = vWB factor through which agonists collagen , thrombin , thromboxanes , ADP induces platelet aggregation • Drugs: 1} Abciximax – treatment of ANGIOPLASTY 2} EPTIFIBTIDE 2} tirofiban
    • 64. GPIIB/IIIA-RECEPTOR ANTAGONISTS – MECHANISM OF ACTION
    • 65. GPIIB/IIIA-RECEPTOR ANTAGONISTS – MECHANISM OF ACTION
    • 66. GPIIB/IIIA-RECEPTOR ANTAGONISTS – MECHANISM OF ACTION
    • 67. GPIIB/IIIA-RECEPTOR ANTAGONISTS – MECHANISM OF ACTION
    • 68. GPIIB/IIIA-RECEPTOR ANTAGONISTS – MECHANISM OF ACTION
    • 69. THROMBOXANE INHIBITORS • Acts through inhibition of thromboxane synthetase = decreases synthesis of TXA2 thus prevents platelet aggregation • Elevates endogenous cAMP in the platelets by inhibiting phosphodiesterase enzyme • Blockade of cellular reuptake of adenosine into platelets ,RBC & endothelial cells =increased extra cellular concentration of adenosine
    • 70. , 1} DIPYRIDAMOLE As synergistic with ASPIRIN With WARFARIN – to decrease the incidence of thromboembolisim in patients with PROSTHETIC HEART VALVES 2}DAZOXIBEN 3}PICOTAMIDE 4}TERUTROBAN
    • 71. MISCELLANEOUS DRUGS • CILOSTAZOL : phosphodiesterase inhibitor = intracellular concentration of cAMP = increase in PK-A = inhibition of platelet aggregation & arterial vasodilator effect Treatment – muscular pains due to cramps , numbness or fatigue • TIMOLOL ( b adrenoceptor blocker ) synergizes action of low dose aspirin • SULFINPYRAZONE uricosuric drug related to phenylbutazone Inhibits COX enzyme = blocks production of prostanoids
    • 72. REFERENCES • H RICHARD ADAMS Veterinary pharmacology and therapeutics, 8th edition. • GOODMAN & GILMAN`S The pharmacological basis of therapeutics, 11th edition. • HS SANDHU Essentials of veterinary pharmacology and toxicology, 2nd edition. • GOOGLE IMAGES • ONLINE SEARCH RELATED TOPICS
    • 73. THANK YOU

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