FA Hematology and Oncology Flashcards
(114 cards)
Heparin Mechanism
Cofactor for the activation of antithrombin, ↓ thrombin, and ↓ factor Xa. Short half-life.
Heparin Use
Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT. Used during pregnancy (does not cross placenta). Follow PTT.
Heparin Toxicity
Bleeding, thrombocytopenia (HIT), osteoporosis, drug-drug interactions. For rapid reversal (antidote), use protamine sulfate (positively charged molecule that binds negatively charged heparin).
Heparin-induced thrombocytopenia (HIT) - development of IgG antibodies against heparin bound to platelet factor 4 (PF4). Antibody-heparin-PF4 complex activates platelets → thrombosis and thrombocytopenia.
Low-Molecular Weight Heparins (LMWHs)
Enoxaparin, dalteparin
Enoxaparin, Dalteparin Mechanism
Compared to regular heparin, act more on factor Xa, have better bioavailability, and 2-4 times longer half-life. Can be administered subcutaneously and without laboratory monitoring. Not easily reversible.
Argatroban, Bivalirudin Mechanism
Derivatives of hirudin, the anticoagulant used by leeches; inhibit thrombin directly.
Argatroban, Bivalirudin Use
Used instead of heparin for anticoagulating patients with HIT.
Warfarin (Coumadin) Mechanism
Interferes with normal synthesis and γ-carboxylation of vitamin K-dependent clotting factors II, VII, IX, and X and proteins C and S. Metabolized by the cytochrome P-450 pathway and ↑ PT. Long half-life.
Warfarin (Coumadin) Use
Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation). Not used in pregnant women (because warfarin, unlike heparin, can cross the placenta). Follow PT/INR values.
Warfarin (Coumadin) Toxicity
Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions.
For reversal of warfarin overdose, give vitamin K. For rapid reversal of severe warfarin overdose, give fresh frozen plasma.
Direct Factor Xa Inhibitors
Apixaban, rivaroxaban
Apixaban, Rivaroxaban Mechanism
Bind and directly inhibit the activity of factor Xa.
Apixaban, Rivaroxaban Use
Treatment and prophylaxis of DVT and PE (rivaroxaban), stroke prophylaxis in patients with atrial fibrillation. Oral agents do not usually require coagulation monitoring.
Apixaban, Rivaroxaban Toxicity
Bleeding (no specific reversal agent available)
Thrombolytics
Alteplase (tPA), reteplase (rPA), tenecteplase (TNK-tPA)
Thrombolytic Mechanism
Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. ↑ PT, ↑ PTT, no change in platelet count.
Thrombolytic Use
Early MI, early ischemic stroke, direct thrombolysis of PE
Thrombolytic Toxicity
Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, or severe hypertension. Treat toxicity with aminocaproic acid, an inhibitor of fibrinolysis. Fresh frozen plasma and cryoprecipitate can also be used to correct factor deficiencies.
Aspirin (ASA) Mechanism [Hem.]
Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation. Platelets cannot synthesize new enzym, so effect lasts until new platelets are produced: ↑ bleeding time, ↓ TXA2 and prostaglandins. No effect on PT or PTT.
Aspirin (ASA) Clinical Use [Hem.]
Antipyretic, analgesic, anti-inflammatory, antiplatelet (↓ aggregation).
Aspirin (ASA) Toxicity
Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye syndrome in children with viral infection. Overdose causes respiratory alkalosis initially, which is then superimposed by metabolic acidosis.
ADP Receptor Inhibitors
Clopidogrel, Ticlopidine, Prasugrel, Ticagrelor
Clopidogrel Mechanism
Inhibit platelet aggregation by irreversibly blocking ADP receptors. Inhibit fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
Clopidogrel Use
Acute coronary syndrome; coronary stenting. ↓ incidence or recurrence of thrombotic stroke.
