Pharm - Hematology and Oncology p 305 - 310
Terms
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Mechanism of
Heparin
(and Enoxaparin) -
Catalyzes the activation of antithrombin 3, decreases thrombin and Xa. Short half-life.
Newer low-molecular weight heparins (enoxaparin) act more on Xa, have better bioavailability and 204 times longer half-life. Can be administered subcutaneously and without laboratory monitoring. Not easily reversible. -
Clinical use of
Heparin -
Immediate anticoagulation for:
-pulmonary embolism
-stroke
-angina
-MI
-DVT.
-used during pregnancy b/c it does not cross the placenta. Follow PTT -
Toxicity of
Heparin
(and treatment of toxicity) -
-Bleeding
-Thrombocytopenia
-Drug-drug interactions
For rapid reversal of heparinization, use PROTAMINE SULFATE ( -
Mechanism of:
Warfarin (Coumadin) -
Interfers with normal synthesis and gamma carboxylation of vitamin K-dependent clotting factors 2, 7, 9, 10, and proteins C & S. Affects EXtrinsic pathway and increases PT.
Long half-life. -
Clinical use of:
Warfarin (Coumadin) -
Chronic anticoagulation
Not used in pregnant women because it crosses the placenta, unlike Heparin.
Follow PT values. -
Toxicity of:
Warfarin (Coumadin) -
-Bleeding
-Teratogenic
-Drug-drug interactions -
4 examples of:
Thrombolytics -
-Streptokinase
-urokinase
-tPA (alteplase)
-APSAC (anistreplase) -
Mechanism of:
Thrombolytics - Directly or indirectly aid conversion of plasminogen to plasmin, the major fibrinolytic enzyme, which cleaves thrombin and fibrin clots.
-
Clinical use: (2)
Thrombolytics -
Early MI
early ischemia stroke -
Toxicity of:
Thrombolytics
(and treatment for it) -
Bleeding.
Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diathesis, or severe hypertension.
Treat toxicity with AMINOCAPROIC ACID, an inhibitor of fibrinolysis -
Mechanism of:
Asprin (ASA) -
Acetylates and irreversibly inhbits cyclooxygenase (both COX-1 and COX-2) to prevent conversion of arachidonic acid to prostaglindins.
Increased bleeding time.
No effect on PT or PTT -
Clinical use: (4)
Asprin (ASA) -
-antipyretic
-analgesic
-anti-inflammatory
-antiplatelet drug -
Toxicity of: (5)
Asprin (ASA) -
-Gastric ulceration
-bleeding
-hyperventilation
-Reye's syndrome
-Tinnitus (CN 8) -
Mechanism of:
Clopidogrel, Ticlopidine -
Inhibits platelet aggregation by irreversibly blocking ADP receptors.
Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa expression -
Clinical use: (3)
Clopidogrel, Ticlopidine -
-Acute coronary syndrome
-coronary stenting
-decreased incidence or recurrence of thrombotic stroke -
Toxicity of: (1)
Clopidogrel, Ticlopidine - Ticlopidine -> Neutropenia