Hematology Flashcards
Heparin
Cofactor for activation of antithrombin, decreases thrombin and decreases factor Xa. Short half-life.
Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT.
Bleeding, thrombocytopenia (HIT), osteoporosis, DDIs. Used during pregnancy (does not cross placenta). Follow PTT.
Rapid reversal (antidote) with protamine sulfate.
Enoxaparin
Cofactor for activation of antithrombin, acts more on factor Xa. Better bioavailability and 2-4x longer half-life.
Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT.
Bleeding, thrombocytopenia (HIT), osteoporosis, DDIs. Used during pregnancy (does not cross placenta). Do not need to follow labs. Not easily reversible.
Dalteparin
Cofactor for activation of antithrombin, acts more on factor Xa. Better bioavailability and 2-4x longer half-life.
Immediate anticoagulation for PE, acute coronary syndrome, MI, DVT.
Bleeding, thrombocytopenia (HIT), osteoporosis, DDIs. Used during pregnancy (does not cross placenta). Do not need to follow labs. Not easily reversible.
Argatroban
Derivative of hirudin, the anticoagulant used by leeches. Inhibits thrombin directly.
Used instead of heparin for anticoagulating patients with HIT.
Bivalirudin
Derivative of hirudin, the anticoagulant used by leeches. Inhibits thrombin directly.
Used instead of heparin for anticoagulating patients with HIT.
Warfarin (Coumadin)
Interferes with normal synthesis and γ-carboxylation of vitamin K-dependent clotting factors, II, VII, XI, and X and proteins C and S. Long half-life.
Metabolized by CYP450 pathway.
Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, prevention of stroke in atrial fibrillation).
Bleeding, teratogenic (do not use in pregnancy, crosses placenta). Follow PT/INR values.
Reversal of overdose with vitamin K. For rapid reversal of severe overdose, give FFP.
Apixaban
Direct factor Xa inhibitor
Stroke prophylaxis in patients with atrial fibrillation
Oral agents do not usually require coagulation monitoring
Bleeding. No specific antidote.
Rivaroxaban
Direct factor Xa inhibitor
Stroke prophylaxis in patients with atrial fibrillation, treatment and prophylaxis of DVT and PE
Oral agents do not usually require coagulation monitoring
Bleeding. No specific antidote.
Alteplase (tPA)
Thrombolytic
Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increases PT and PTT, no change in platelet count
Early MI, early ischemic stroke, direct thrombolysis of severe PE
Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, severe hypertension.
Treat toxicity with aminocaproic acid, inhibitor of fibrinolysis. FFP and cryoprecipitate can also be used to correct factor deficiencies.
Reteplase (rPA)
Thrombolytic
Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increases PT and PTT, no change in platelet count
Early MI, early ischemic stroke, direct thrombolysis of severe PE
Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, severe hypertension.
Treat toxicity with aminocaproic acid, inhibitor of fibrinolysis. FFP and cryoprecipitate can also be used to correct factor deficiencies.
Tenecteplase (TNK-tPA)
Thrombolytic
Directly or indirectly aid conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increases PT and PTT, no change in platelet count
Early MI, early ischemic stroke, direct thrombolysis of severe PE
Bleeding. Contraindicated in patients with active bleeding, history of intracranial bleeding, recent surgery, known bleeding diatheses, severe hypertension.
Treat toxicity with aminocaproic acid, inhibitor of fibrinolysis. FFP and cryoprecipitate can also be used to correct factor deficiencies.
Aspirin (ASA)
Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) enzyme by covalent acetylation. Platelets cannot synthesize new enzyme, so effects last until new platelets are produced. Increases bleeding time, decreases TXA2 and prostaglandins. No effects on PT/PTT.
Antipyretic, analgesic, anti-inflammatory, antiplatelet (decreases aggregation).
Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, upper GI bleeding. Reye syndrome in children with viral infection. Overdose causes respiratory alkalosis initially, which is then superimposed by metabolic acidosis.
Clopidogrel
ADP receptor inhibitor
Inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding fibrinogen.
Acute coronary syndrome, coronary stenting, decreased incidence of recurrence of thrombotic stroke
TTP/HUS may be seen.
Ticlodipine
ADP receptor inhibitor
Inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding fibrinogen.
Acute coronary syndrome, coronary stenting, decreased incidence of recurrence of thrombotic stroke
Neutropenia. TTP/HUS may be seen.
Prasugrel
ADP receptor inhibitor
Inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding fibrinogen.
Acute coronary syndrome, coronary stenting, decreased incidence of recurrence of thrombotic stroke
TTP/HUS may be seen.
