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• Aspirin


  COX-2 inhibitor that irreversibly blocks conversion of arachidonic acid to prostaglandin endoperoxide H2 in platelets, resulting in inhibition of TXA2 synthesis
• TXA2


  • Constricts vascular smooth muscle
  • Inhibits activation of platelets
  • Inhibits aggregation of platelets
  • Reduced levels increase the risk of ischaemic stroke
• Aspirin action


  • TXA2 synthesis recovers in affected platelets after 7-10 days
  • TXA2 synthesis is blocked for the life-span of the platelets exposed to the drug
  • Aspirin blocks synthesis of new protein in platelets
  • Aspirin may induce a bronchodilation
• Contraindications for Aspirin


  • Children under 16 years
  • Severe cardiac failure
  • Past history of peptic ulcer
  • Haemophilia
  • Following coronary by-pass surgery
• Clopidogrel


  • Inhibits platelet aggregation and used in the prevention of atherothrombotic events
  • Irreversible blocker of P2Y12 receptors
• Clopidogrel taken with omeprazole


  The risk of thrombus formation is increased compared to when Clopidogrel is taken alone
• Glycoprotein IIB/IIIA receptor antagonists


  • Inhibit platelet GPIIb/IIIa receptors and may be used in high-risk patients who require angioplasty
  • Administered intravenously
• Vitamin K deficiency


  May lead to excessive bleeding (e.g. haemorrhagic disease of the newborn)
• Warfarin


  Vitamin K antagonist that may lead to excessive bleeding if used excessively due to inactivation of Vitamin K dependent clotting factors
• Factors that enhance the effect of Warfarin

  • Amiodarone
  • Metronidazole
  • Co-trimoxazole
• Factors that do not enhance the effect of Warfarin


  • Rifampicin
  • Carbamazepine
  • Increased hepatic synthesis of proteins (e.g. Pregnancy)
  • Liver disease
• Heparin-induced thrombocytopenia


  Reducing platelet count increases the risk of thrombus formation
• Switching from Warfarin to Rivaroxaban


  There should be a delay in starting the rivaroxaban until the INR value returns to it's target value
• Plasminogen is an inactive precursor of plasmin
• Plasminogen is found in circulating blood in it's activation-resistant form
• Plasminogen activators are unstable in circulating blood
• Plasminogen is inactivated once inside a formed thrombus
• Incorrect responses about fibrinolytic drugs

  • Streptokinase is inactivated several days after administration due to antibody production
  • Alteplase effects can be reversed by tranexamic acid
  • Alteplase is more effective against plasma plasminogen compared to fibrin bound plasminogen
  • Streptokinase and alteplase are inactivated if administered orally
• Clinical uses of alteplase

  • Gastric ulcers
  • Haemorrhagic stroke
  • Thrombotic stroke
  • Uncontrolled hypertension
  • Pregnancy
• Cautions for clinical use of alteplase

  • Atrial fibrillation
  • Pulmonary embolism
  • Acute myocardial infarction
  • Removal of thrombi occluding central veinous access