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| Clinical effects of Factor XII deficiency | none
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| Describe the clinical bleeding associated with von Willebrand's disease | mucosal bleeding(epistaxis, menorrhagia, GI bleed), excessive bruising, or bleeding after minor trauma
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| Describe the clinical bleeding associated with platelet disorders | mucosal bleeding(epistaxis, menorrhagia, GI bleed), excessive bruising, or bleeding after minor trauma
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| Describe the bleeding associated with hemophilia | Bleeding into joints, muscles or soft tissues
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| The most common causes of primary fibrinolysis | Severe liver disease and hepatic surgery
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| In non-bleeding patients with thrombocytopenia caused by marrow failure, prophylactic platelet transfusions are generally reserved for platelet counts less than this number | 10K
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| This syndrome is due to deficiency of GPIb/IX in platelets | Bernard-Soulier
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| This syndrome is due to deficiency of GPIIb/IIIa in platelets | Glanzmann thrombasthenaa
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| This drug has been effective treating bleeding associated with uremia | DDAVP(desmopressin)
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| Describe the underlying pathophysiology of the most common type of von Willebrand's disease | Type 1 vWD has mild to moderate quantitative deficiency of vWF
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| In this type of von Willebrand's disease, vWF is virtually absent along with Factor VIII | Type 3 vWD
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| These lysine analogues are used as anti-fibrinolytics | epsilon aminocaproic acid and tranexamic acid
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| Mechanism of action of tranexamic acid and epsilon aminocaproic acid | interfere with plasmin binding to fibrin, thereby inhibiting fibrinolysis (anti-fibrinolytics)
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| This site of bleeding is a contraindicationto tranexamic acid and EACA | upper urinary tract bc obstruction may result from failure of clot lysis
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| X-linked congenital bleeding disorder caused by Factor VIII deficiency | Hemophilia A
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| Products of choice in Hemophilia A | Recombinant Factor VIII
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| FDA requires that each unit of cryoprecipitated AHF contain this much factor VIII | 80 IU
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| DDAVP and cryo can be useful in the treatment of: A. Hemophilia A B. Hemophilia B C. Both D. Neither | A.
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| What is the mainstay of therapy for hemophilia patients with inhibitors to factor VIII or IX? | activated Prothrombin complex concentrates (aPCC) or recombinant Factor VIIa (rFVIIa)
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| Treatment of choice for Factor V deficiency | plasma
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| Treatment for Factor XII deficiency | none
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| This deficiency is associated with umbilical stump bleeding | Factor XIII
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| Treatment for alpha2-plasmin inhibitor deficiency | epsilon aminocaproic acid (EACA)
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| Vitamin K dependent coagulation factors | II,VII,IX, X
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| Warfarin-induced skin necrosis is related to the drug's early effect on this | protein C synthesis
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| If patient has serious bleeding on warfarin, this product is recommended | 4-factor (II,VII,IX,X) Prothrombin complex concentrate (PCC)
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| Calculation for FFP units needed to reverse heparin effect | plasma is not effective in reversing heparin effect
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| Drug used to reverse heparin effect | protamine sulfate
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| This drug is a synthetic pentasaccharide that strongly binds anti-thrombin and acts as a selective inhibitor to Factor Xa | Fondaparinux
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| This drug is an oral targeted thrombin inhibitor | Dabigatran (Pradaxa)
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| These drugs are oral targeted Factor Xa inhibitors | Rivaroxaban (Xarelto) and Apixaban (Eliquis)
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| These drugs selectively inhibit ADP-induced activation of platelets via irreversible alteration of the platelet P2Y12 receptor | Clopigrodel (Plavix) and Prasugrel (Effient)
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| This is a synthetic analogue of vasopressin | DDAVP
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| These factors are released from endothelial cells when DDAVP is given | vWF, Factor VIII, and tPA
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| These antifibrinolytic drugs are synthetic analogues of lysine | EACA and Tranexamic acid
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| Mechanism of action of tranexamic acid | occupies lysine binding sites of plasminogen and plasminogen activators which delays clot resorption
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| This is the most important protease inhibitor of activated coagulation factors and is central to the in-vivo effect of heparin | antithrombin
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| Condition in infants with homozygous deficiency of protein C or S | purpura fulminans
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| When does "warfarin induced skin necrosis occur"? | When patients with protein C or S deficiency are started on warfarin
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| This is the specific antibody epitope in anti-phospholipid syndrome | beta-2 glycoprotein I
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| Clinical effect of "Lupus anti-coagulant" | thrombosis
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| Lab criteria for Lupus anticoagulant | 1. prolonged PTT 2. prolonged Russell viper venom test 3. fails to correct on 1:1 mixing study 4. corrects when excess phospholipid is added
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| This is a drug associated ITP disorder characterized by paradoxical thrombosis | HIT: heparin induced thrombocytopenia
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| These tests are used to confirm a dx of HIT | antibodies to platelet factor 4/heparin complexes or serotonin release assay
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| Platelet dose for a patient with HIT and a platelet count of 19,000 | none. avoid platelet transfusion in this dx
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| The majority of adult-onset cases of TTP have a deficiency of this protein | ADAMTS13
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| Outline treatment of TTP if TPE is not readily available | FFP at 40ml/kg until TPE can be arranged
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| Etiology of Typical hemolytic uremic syndrome (HUS) | shiga toxin producing E. coli
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| Best treatment for atypical HUS | eculizamab, C5 monoclonal antibody, disease results from excessive activation of alternative complement pathway
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