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32 Cards in this Set

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