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Lecture

Antiplatelets and Anticoagulants.docx

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Department
Nursing
Course
NURS 2050
Professor
Cynthia Barkhouse Mckeen
Semester
Fall

Description
Antiplatelets and Anticoagulants Purpose: prevent formation of growing of thrombi or help the body while it works to dissolve formed thrombi. **they do not lyse clots Antiplatelets 1. Cyclooxygenase inhibitors (e.g. ASA) 2. Adenosine Diphosphate (ADP) Receptor Antagonists (e.g Clopidogrel) 3. Glycoprotein IIb/IIIa receptor antagonists (e.g. Abciximab, Eptifibatide, Tirofiban) Anticoagulants 1. Vitamin K antagonists- (e.g. Warfarin- a.k.a. Coumadin) 2. Factor Xa and thrombin (IIa) inhibitors- (e.g. Heparin)  Selective Factor Xa inhibitors (e.g Fondaparinux, Rivaroxaban) 3. Direct thrombin (IIa) inhibitors (e.g. Argatroban, Lepirudin, Dabigatran) 1. Vitamin K antagonist- Warfarin (coumadin) Oral anticoagulant • Available in many different strengths • Affects synthesis of vitamin K dependent clotting factors • VII, IX, X, prothrombin (II) (i.e. 2, 7, 9, 10) • Vitamin K dependent clotting factors  NOTE THAT PROTEIN C AND S ARE VITAMIN K DEPENDENT • Delayed effect on coagulation ***No effect on clotting factors already formed • Overlap with heparin in certain situations • Variable half life in clotting factors 6 hours to 2.5 days o Need to consider drug AND clotting factor t1/2 • Prolonged effect after stopping  long t1/2 of drug - 1.5 – 2 days  Monitoring INR (PT ratio multiplied by a correction factor) - Outpatient monitoring of INR Adverse effects • Hemorrhage, bleeding (important counselling) Interactions (drug-drug, drug-food, etc) Pharmacokinetic drug-drug – enzyme inhibition or induction E.g. Amiodarone, analgesics, antibiotics, antidepressants Pharmacodynamic interactions – e.g. vitamin K Drugs can: Increase effects of warfarin, Promote bleeding Decrease the effects of warfarin, Potentially lead to thromboembolic events Antidote to overdose  Vitamin K1 (phytonadione) • Given po when possible 2. Factor Xa and thrombin (IIa) inhibitors- Heparin  Heparin-AT complex:  Antithrombin inhibits clotting factors:  Factors IIa (thrombin), Xa, IXa, XIa, XIIa  Factors IIa and Xa are the most responsive to inhibition. (Heparin - Anti IIa > anti-Xa activity). ADME & Other Considerations • Not absorbed (polarity and size) – IV infusion and SC • Does not cross placenta* • Can bind to other tissues and proteins  M,E – undergoes metabolism and renal excretion • T1/2 – 1.5 hours (organ dysfunction = prolonged t1/2) Adverse effects • Hemorrhage • Hypersensitivity • HIT (heparin induced thrombocytopenia) • Platelet aggregation -Paradoxical in coagulation Antiplatelet antibodies • Osteoporosis – suppression osteoblastic, activation osteoclastic to promote bone loss - -long term LMWHS (THE “PARINS”)  Shorter molecule than regular heparin  Fixed dosing schedule and weight based dosing  Longer half life (once daily to bid dosing)  SC only  No monitoring of aPTT –Xa level instead but these are not routinely measured  Anti Xa greater than anti ii activity Adverse Effects:  Bleeding  Thrombocytopenia is much less Thrombolytics  (e.g. Alteplase, Streptokinase, Reteplase, Tenecteplase) • Act to via plasminogen to enhance the activity of plasmin • Side effects – bleeding! • Use in acute care, special circumstances E.g. stroke, MI HEMOSTASIS – Process to stop bleeding  Stage 1 — formation of platelet plug- Platelet aggregation  Stage 2 — plug/coagulation reinforcement (production of fibrin) - Fibrin is produced by way of 2 convergent pathways: Intrinsic and Extrinsic system (aka tissue factor pathway) Body’s defence against coagulation • Antithrombin III (antithrombin)- Protein that complexes with stray clotting factors • Plasmin- enzyme that digests fibrin meshwork of clot, Plasminogen is its precursor • Protein C and S COX 1  At sites of injury COX catalyzes the synthesis of PGE2
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