Phils Hemo Coag
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| Five reasons to reject coag specimens | >2 hours at room temp, exposure to temp extremes, tube <90% full, clotted specimen, or hemolyzed specimen
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| Sodium citrate should be used. labile factors are preserved better | incorrect anticoag
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| tissue thromboplastin activates coagulation and shortens times is caused by | probing for vein
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| need nine parts of blood to one part of anticoagulant tubes less than 90% full will have longer times | incorrect ratio of blood to anticoag
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| due to this the blood will clot | failure to mix anticoag with blood
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| this is what it means when hematocrits above 55% lead to longer times and anticoag must be reduced | polycythemia
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| hemolyzed rbcs may activate clotting factors and interfere with photometric readings | hemolysis
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| this may interfere with photo-optical methods and should be tested with electromechanical instruments | lipemia
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| sample should remain capped to preven change in pH. Test within 2 hours if stored at room temp or 4 if stored at 4 C loss of labile factors will prolong times | Improperstorage
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| running controls on each shift will verify system performance | improper storage or reconstitution of reagents, equipment malfunction
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| What are the three stages of hemostasis | primary, secondary, fibrinolysis
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| In this stage there is vasoconstriction, platelet adhesion to exposed subendothelial connective tissue, platelet aggregation to form initial plug at injury site | primary hemostasis
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| in this stage of hemostasis the coagulation factors interact on platelet surface to produce fibrin, fibrin is stabilized by factor XIII | secondary hemostasis
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| in this stage the release of tissue plasminogen activator, conversion of plasminogen to plasmin, conversion of fibrin to fibrin degradation products | fibrinolysis
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| What factors are involved with the extrinsic pathway | VII
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| What is used to evaluate the extrinsic pathway | PT
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| What factors are involved with the intrinsic pathway | XII, XI, IX, VIII
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| What is used to evaluate the intrinsic pathway | APTT
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| What factors are involved with the common pathway | X, V, II, I
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| Which factors are produced in the liver | all of them
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| the von willebrand's portion of factor VIII is produced where else | endothelial cells and megakaryocytes
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| Which factors require Vit K for synthesis | II, VII, IX, X
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| Which factors are in the prothrombin group | II, VII, IX, X
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| Which factors are affected by coumadin | II, VII, IX, X
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| Which factors are consumed by clotting | I, II, V, VIII, XIII
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| which factors are labile | V and VIII
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| Which factors are the contact group | Prekallikrein, HMW kininogen, XII, XI
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| Factors in the extrinsic pathway | III, VII
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| Factors in the intrinsic pathway | Rekalikrein, HMW kininogen, XII, XI, IX, VIII
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| Factors in the common pathway | X, V, II, I
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| Afibrinogenemia, hypofigrinogenemia, dysfibrinogenemia are all associated with a deficiency of what factor | I
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| What is the treatment for someone with a deficiency of factor I | cryoprecipitate
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| Prothrombin deficiency is associated with what factor | II
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| How is prothrombin deficiency treated | FFP
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| Labile factor deficiency is an autosomal recessive disease associated with what factor | V
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| How is labile factor deficiency treated | FFP
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| How is Factor VII deficiency treated | plasma or prothrombin complex
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| this is one of the most common inherited coagulation disorders, it is sex linked recessive, occurs primarily in males, mothers are carriers | Hemophilia A
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| What factor is linked to hemophilia A | VIII
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| What factor is associated with Von Willebrand's disease | VIII
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| THis is one of the most common inherited coag disorders, a deficiency of vW portion of Factor VIII, with both sexes affected and problems with platelets | Von Willebrand's disease
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| How is Hemophilia A treated | cryoprecipitate, factor VII conc. DDAVP
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| How is Von Willebrand's disease treated | Cryoprecipitate or DDAVP
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| what factor is associated with hemophilia B which is a sex linked recessive disease | IX
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| How is hemophilia B treated | plasma or commercial con.
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| What factor is associated with Stuart prower factor deficiency | X
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| How is stuart prower factor deficiency treated | FFP or prothrombin conc
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| What factor is associated with hemophilia C | XI
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| How is hemophilia C treated | FFP
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| What factor is associated with Hageman trait | XII
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| What is the treatment for Hageman trait | none there is no bleeding disorder
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| What factor is associated with fibrin stabilizing factor deficiency | XIII
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| How is fibrin stabilizing factor deficiency treated | plasma, lyophilized placental factor XIII
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| What factors are affected by mild liver disease | II, VII, IX, X
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| What factors are affected by moderate liver disease | II, VII, IX, X, V, VIII
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| What factors are affected by severe liver disease | II, VII, IX, X, V, VIII, I
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| What factors are affected by vitamin K deficiency | II, VII, IX, X
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| What factors are affected by coumadin therapy | II, VII, IX, X
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| What factors are affected by disseminated intravasular coagulation | I, II, V, VIII, and platelets
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| What factors are affected by primary fibrinolysis | I, V, VIII
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| This test's significance is that prolonged with platelet abnormalities, vasular disease. prolonged by asprin measuring function of factor VIII | Bleeding time
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| This test's function is a test of platelet adhesion, aggregation, and secretion. detects qualitative platelet defects | Platelet aggregation
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| This test detects deficiencies in extrinsic and common pathways used to monitor coumadin therapy is reported in INR and factors measured VII, X, V, II, I | Prothrombin time (PT)
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| this test detects deficiencies in the intrinsic and common pathways, most common test to monitor heparin therapy | Activated partial throboplastin time (APTT)
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| this test is used very little to monitor heparin therapy (fibrinogen in common pathway) | Thrombin time (TT)
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| This test is a Factor XIII screening test | Urea solubility
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| this test is positive in DIC, Deep vein thrombosis, pulmonary embolism, and after lytic therapy, but negative in primary fibrinolysis | D-dimer
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| this is the precursor of plasmin, is decreased following lytic therapy, DIC, and primary fibrinolysis | plasminogen
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| Hepran cofactor, deficiencys associated with thrombosis | Antithrombin III
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| Inhibitors of coagulation deficiencies associated with thromboembolic disorders | Protein C and S
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| This deficiency has a normal PT, abnormal APTT, is corrected by absorbed plasma, not corrected with aged serum | Factor VIII
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| This deficiency has a normal PT, abnormal APTT is corrected by Aged serum, not corrected by adsorbed plasma | Factor IX
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| This deficiency has normal PT, abnormal APTT is corrected by both aged serum and absorbed plasma | XI
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| This deficiency has normal PT, abnormal APTT, and is corrected by aged serum and adsorbed plasma | factor XII
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| This deficiency has an abnormal PT and APTT, and is corrected by adsorbed plasma, not corrected by aged serum | factor I
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| This deficiency has an abnormal PT and APTT, and is not corrected by Aged serum and adsorbed plasma | Factor II
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| This deficiency has an abnormal PT and APTT and is corrected by adsorbed plasma, not corrected by aged serum | V
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| This deficiency has an abnormal PT and APTT and is corrected by aged serum, not corrected by adsorbed plasma | factor X
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| Adsorbed serum corrects which factors | V, VIII, XI, XII
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| Aged plasma corrects which factors | VII, IX, X, XI, XII
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| What disease is associated with the following findings Decreased Factor VIII APTT prolongs PT normal Bleeding time Normal Platelet count normal | Hemophilia A
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| What disease is associated with these lab findings APTT prolonged PT normal Bleeding time normal Platelet count normal | Hemophilia B
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| What disease is characterized by these lab findings Bleeding time prolonged Platelet aggregation abnormal w/ristocetin Factor VIII may be decreased APTT prolonged PT normal Platelet count normal | Von Willebrand's disease
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| What disease is associated with these findings Clot retraction abnormal bleeding time prolonged platelet count normal platelet aggregation abnormal with ADP, collagen, thrombin, epinephrin | Glanzmann's Thrombasthenia
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| What disease is associated with these findings bleeding time prolonged giant platelets platelet cound decreased clot retraction normal | Bernard Soulier syndrome
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| What are the key differences in DIC and primary fibrinolysis | Platelets, D-Dimer, Antithrombin III, and RBC Morphology
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| this anticoagulant is administered subcutaneously or IV has an antithrombin effect immediately is short acting Monitored by APTT Reversed by protamine sulfate Requires AT-III to be effective | Heparin
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| This anticoagulant is administered orally Acts as Vit K antagonist Slow acting Long duration Monitored by PT Reversed by Vit K Decreases the production of II, VII, IX, X | Coumadin
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| the purpose of this therapy is the activate fibinolytic system, is used to treate acute myocardial infarction, deep vein thrombosis, and pumonary emboli | thrombolytic therapy
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| What drugs are used in thrombolytic therapy | strptokinase, urokinase, tissue plasminogen activator, prourokinase, acylated plasminogen streptokinase actvated complex
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| What changes are induced by thrombolytic therapy | decrease in fibrinogen, plasminogen, V, VII, IX, XII
increase in plasmin, FDP, D-dimer, APTT, PT, TT
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