Anticoagulants

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meganc0201
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39915
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Anticoagulants
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2010-10-05 14:07:07
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Anticoagulants
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Pharm: Anticoagulants
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  1. Component involved in clot formation:
    Vasocontriction
  2. · Inhibition of prostacyclin (PGI2) synthesis in endothelial cells. ( Prostacyclin normally will promote dilation of the blood vessel.)
  3. · Increase in serotonin which causes vasoconstriction.
  4. Component involved in clot formation:
    Platelet Aggregation-platelet plug formation
  5. · stimulated by exposed collagen contact with blood platelets
  6. · release of ADP and thromboxaneA2 from "activated platelets"
  7. · formation of plug or thrombus
  8. Component involved in clot formation:
    Intristic Coagulation Pathway
  9. ·initiated by contact of clotting factor XII (from liver) with collagen
    • ·pathway is a series of sequential reactions that convert inactive coagulation factors synthesized in the liver to active ones
    • ·monitored by aPTT, activated partial thromboplastin time
  10. Component involved in clot formation:
    Extrinsic Coagulation Pathway
  11. ·activated by thromboplastin (tissue release factor) released from damaged tissue (collagen exposed)
    ·monitored by PT, prothrombin time, or International Normalized Ratio, INR (most often used)
  12. Four major groups of Anticoagulant or Thrombolytic Drugs or Antiplatelet Drugs
    • 1. Injectable anticoagulants: heparin and low molecular weight heparins (LMW)
    • 2. Oral anticoagulants: warfarin
    • 3. Thrombolytic (clot dissolving): streptokinase and tPA (dissolve clot for fibrin)
    • 4. Antiplatelet (antiplatelet aggregation): acetylsalicylic acid, clopidogrel, abciximab
    • Prevent fibrin formation
  13. Injectable Anticoagulants:
    Heparin
    a. Pharmacodynamics, mechanism of action—a large negatively charged molecule that combines with the endogenous antithrombin III. This complex then promotes the destruction of factors such as Xa and thrombin

    b. Pharmacokinetics - intermittent IV, continuous IV, SC (deep fat), not IM or oral. (does not cross the placenta)

    • c. Types of treatment.
    • (1) prevention of venous thrombosis
    • (2) atrial fibrillation
    • (3) phlebitis
    • (4) cardiac or vascular surgery

    • d. Toxicity, side effects
    • (1) Hemorrhage - treatment - protamine (small positively charged molecule) (neutralizes heparin)
    • (2) Osteoporosis (long term use)
    • (3) Alopecia (long term use)
    • (4) Thrombocytopenia (lack of platelets) (HIT: heparin induced thrombocytopenia watch for decreased platelets)
    • (5) Allergic reactions
  14. Injectable Anticoagulants:
    Enoxaparin
    • (smaller particles of heparin)--LMW heparin—binds only to Xa not thrombin. Self administration (subcutaneously), less incidence of thrombocytopenia and does not require daily monitoring.
    • --longer half life than heparin--> allows for home therapy
  15. Oral Anticoagulants:
    Warfarin
    a. Pharmacodynamics, mechanism of action - competitive inhibitor of vitamin K-dependent synthesis of inactive clotting factors II, VII, IX, X.
  16. b. Pharmacokinetics—becomes active only after active clotting factors have been degraded. (4-5 days)
  17. a) well absorbed by oral route
    • b) 99% bound to plasma albumin
    • c) metabolized in liver
  18. c. Side effects - toxicity
  19. (1) hemorrhage
    • (2) deformities in the fetus
    • (3) tissue necrosis
  20. d. Drug interactions
  21. - Synergists (potentiate effects)
    • (1) acetylsalicylic acid (aspirin)
    • (2) antibiotics (broad spectrum)
    • (3) Vitamin E
    • - Antagonists
    • (1) barbiturates
    • (2) vitamin K (especially food-tomatoes, dark leafy vegetables, bananas, fish)
    • (3) estrogens
  22. f. Treatment of toxicity - phytonadione (vitamin K1), plasma transfusion
  23. Thrombolytic Agents
    • (Dissolve Clots)
    • Plasminogen is converted to plasmin by t-PA (tissue plasminogen activator) on the site of the clot. Freely circulating plasminogen can also be converted to plasmin, but in this freely circulating form, plasmin is a relatively nonspecific serine protease (or enzyme that breaks down protein) and thus will also break down other clotting factors such as fibrin, fibrinogen, V, VIII, and XII in a nonspecific fashion (not clot specific).
  24. Thrombolytic Agents:
    Streptokinase
    • Mechanism of Action:
    • Forms a complex with circulating plasminogen and catalyzes the conversion of plasminogen to plasmin which digests circulating fibrinogen and fibrin in thrombi (lacks fibrin, or clot specificity)
    • Source:
    • Strept. culture
    • Adverse Reaction:
    • Allergic and Bleeding
    • Half-Life: 12-18 min
  25. Thrombolytic Agent:
    Alteplase (t-PA or rt-PA)
    • Mechanism of Action:
    • Forms a complex with fibrin bound plasminogen and catalyzes the conversion of plasminogen to plasmin directly on the clot.(Is fibrin or clot specific)
    • Source:
    • human tissue-type plasminogen activator
    • Adverse Reaction:
    • Bleeding
    • Half-life:
    • 2-6 min
  26. Characteristics of thrombolytic therapy
    acute myocardial infarction (within 3 hours), acute venous thrombosis, pulmonary embolism, cerebral embolism (within 3 hours-ischemic stroke)
  27. Antiplatelt Drugs
  28. a. acetylsalicylic acid (aspirin)
  29. b. clopidogrel (older drug with more side effects)
  30. c. abciximab
  31. Anti-platelet Drugs:
    Acetylsalicylic acid (aspirin)
    • inhibition of platelet aggregation: mechanism of action
    • Irreversible inhibition of cyclooxygenase (COX-1) and thus inhibiting the synthesis of
    • thromboxane A2 in platelets.
    • Effective for about a week until new platelets are synthesized.
  32. Antiplatelet Drugs:
    Clogidogrel
    • inhibition of platelet aggregation
    • mechanism of action – blocks ADP receptors (receptors which stimulate platelet
    • aggregation in the presence of ADP). Takes several days for peak action.
  33. Antiplatlet Drugs:
    Abciximab
    • inhibition of platelet aggregation
    • Mechanism of action—An antibody which binds to platelets at the fibrinogen receptors
    • (glycoprotein IIb/IIIa receptors ,and thus prevents binding of fibrinogen which in turn prevents platelet aggregation.

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