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32 Cards in this Set
- Front
- Back
PT - pathway tested and factors
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Tests extrinsic pathway; I, II, V, VII, X
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PTT - pathway tested and factors
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Tests intrinsic pathway; all factors except VII, XIII
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Hemophilia A/B - deficiency and clinical signs
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A: VIII deficiency ,B: IX deficiency; hemarthroses, easy bruising
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Hemophilia A/B PT and PTT times
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PT normal, PTT increased (extrinsic factors affected)
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Vit K deficiency - enzyme and factors affected
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Epoxide reductase; II, VII, IX, X, C, S
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Vit K deficiency PT and PTT times
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PT increased, PTT increased (general clotting factor deficiency)
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Bernard-Soulier features and lab values
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Gp Ib deficiency - defect in platelet-vWF adhesion, no platelet plug; PC decreased, BT increased
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Glanzmann's thrombasthenia
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Gp IIb/IIIa deficiency - no platelet-platelet aggregation
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Glanzmann's thrombasthenia PC and BT values
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PC: normal
BT: increased |
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Idiopathic thrombocytopenic purpura (ITP)
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Anti-Gp IIb/IIIa antibodies; splenic macrophages destroy platelet-antibody complex; PC decreased, BT increased
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Thrombotic thrombocytopenic purpura (TTP)
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vWF metalloprotease deficiency; increased platelet aggregation, thombosis; decreased PC, increased BT
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Glanzmann's thrombasthenia - lab findings
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Blood smear with no platelet clumping
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ITP characteristic lab findings
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Increased megakaryocytes
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TTP characteristic lab findings
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Schistocytes, increased LDH
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TTP symptoms (5)
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Neurologic, kidney symptoms, fever, thrombocytopenia, microangiopathic hemolytic anemia
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von Willibrand's disease
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Most common, autosomal dominant; vWF deficiency - defect in platelet-vWF adhesion, intrinsic pathway defect (vWF carries factor VIII)
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von Willibrand's disease diagnostic assay
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Ristocetin cofactor assay
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von Willibrand's treatment
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DDAVP (desmopressin) - releases vWF from endothelium
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von Willibrand's PC/BT/PT/PTT values
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PC: normal; BT: increased; PT: normal; PTT: normal/increased
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DIC
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Widespread clotting activation leading to clotting deficiency, massive hemorrhage
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DIC PC/BT/PT/PTT values
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PC: decreased; BT: increased; PT: increased; PTT: increased
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DIC causes ("STOP Making New Thrombi")
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Sepsis, Trauma, Obstretics, Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion
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DIC lab findings
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Schistocytes, D-Dimers (fibrin split products), decreased fibrinogen, decreased V and VIII
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Factor V Leiden
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Factor V resistant to degradation by Protein C; most common inherited hypercoagulability
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Prothrombin gene mutation
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Mutation in 3' untranslated region --> Prothrombin production --> Venous clots
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Antithrombin deficiency
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Hypercoagulatbility state; PTT rise is blunted after heparin
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Protein C+S deficiency
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Decreased V, VIII inactivation; Increased thrombotic skin necrosis with hemorrhage after warfarin administration
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Packed RBC effect, clinical use
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Increase Hb, O2 capacity; acute blood loss, severe anemia
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Transfused platelets clinical use
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Stop significant bleeding
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Fresh frozen plasma effect and clinical use
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Increase coagulation factor levels; DIC, cirrhosis, warfarin overdose
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Cryoprecipitate effect and clinical use
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Contains fibrinogen, VIII, XIII, vWF, fibronectin; treat coagulation factor deficiencies
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Blood transfusion risks
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Infection (low), transfusion reactions, Fe overload, hypocalcemia, hyperkalemia
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