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Phils Hemo Coag
| Question | Answer |
|---|---|
| Five reasons to reject coag specimens | >2 hours at room temp, exposure to temp extremes, tube <90% full, clotted specimen, or hemolyzed specimen |
| Sodium citrate should be used. labile factors are preserved better | incorrect anticoag |
| tissue thromboplastin activates coagulation and shortens times is caused by | probing for vein |
| 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 |
| due to this the blood will clot | failure to mix anticoag with blood |
| this is what it means when hematocrits above 55% lead to longer times and anticoag must be reduced | polycythemia |
| hemolyzed rbcs may activate clotting factors and interfere with photometric readings | hemolysis |
| this may interfere with photo-optical methods and should be tested with electromechanical instruments | lipemia |
| 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 |
| running controls on each shift will verify system performance | improper storage or reconstitution of reagents, equipment malfunction |
| What are the three stages of hemostasis | primary, secondary, fibrinolysis |
| In this stage there is vasoconstriction, platelet adhesion to exposed subendothelial connective tissue, platelet aggregation to form initial plug at injury site | primary hemostasis |
| in this stage of hemostasis the coagulation factors interact on platelet surface to produce fibrin, fibrin is stabilized by factor XIII | secondary hemostasis |
| in this stage the release of tissue plasminogen activator, conversion of plasminogen to plasmin, conversion of fibrin to fibrin degradation products | fibrinolysis |
| What factors are involved with the extrinsic pathway | VII |
| What is used to evaluate the extrinsic pathway | PT |
| What factors are involved with the intrinsic pathway | XII, XI, IX, VIII |
| What is used to evaluate the intrinsic pathway | APTT |
| What factors are involved with the common pathway | X, V, II, I |
| Which factors are produced in the liver | all of them |
| the von willebrand's portion of factor VIII is produced where else | endothelial cells and megakaryocytes |
| Which factors require Vit K for synthesis | II, VII, IX, X |
| Which factors are in the prothrombin group | II, VII, IX, X |
| Which factors are affected by coumadin | II, VII, IX, X |
| Which factors are consumed by clotting | I, II, V, VIII, XIII |
| which factors are labile | V and VIII |
| Which factors are the contact group | Prekallikrein, HMW kininogen, XII, XI |
| Factors in the extrinsic pathway | III, VII |
| Factors in the intrinsic pathway | Rekalikrein, HMW kininogen, XII, XI, IX, VIII |
| Factors in the common pathway | X, V, II, I |
| Afibrinogenemia, hypofigrinogenemia, dysfibrinogenemia are all associated with a deficiency of what factor | I |
| What is the treatment for someone with a deficiency of factor I | cryoprecipitate |
| Prothrombin deficiency is associated with what factor | II |
| How is prothrombin deficiency treated | FFP |
| Labile factor deficiency is an autosomal recessive disease associated with what factor | V |
| How is labile factor deficiency treated | FFP |
| How is Factor VII deficiency treated | plasma or prothrombin complex |
| this is one of the most common inherited coagulation disorders, it is sex linked recessive, occurs primarily in males, mothers are carriers | Hemophilia A |
| What factor is linked to hemophilia A | VIII |
| What factor is associated with Von Willebrand's disease | VIII |
| 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 |
| How is Hemophilia A treated | cryoprecipitate, factor VII conc. DDAVP |
| How is Von Willebrand's disease treated | Cryoprecipitate or DDAVP |
| what factor is associated with hemophilia B which is a sex linked recessive disease | IX |
| How is hemophilia B treated | plasma or commercial con. |
| What factor is associated with Stuart prower factor deficiency | X |
| How is stuart prower factor deficiency treated | FFP or prothrombin conc |
| What factor is associated with hemophilia C | XI |
| How is hemophilia C treated | FFP |
| What factor is associated with Hageman trait | XII |
| What is the treatment for Hageman trait | none there is no bleeding disorder |
| What factor is associated with fibrin stabilizing factor deficiency | XIII |
| How is fibrin stabilizing factor deficiency treated | plasma, lyophilized placental factor XIII |
| What factors are affected by mild liver disease | II, VII, IX, X |
| What factors are affected by moderate liver disease | II, VII, IX, X, V, VIII |
| What factors are affected by severe liver disease | II, VII, IX, X, V, VIII, I |
| What factors are affected by vitamin K deficiency | II, VII, IX, X |
| What factors are affected by coumadin therapy | II, VII, IX, X |
| What factors are affected by disseminated intravasular coagulation | I, II, V, VIII, and platelets |
| What factors are affected by primary fibrinolysis | I, V, VIII |
| This test's significance is that prolonged with platelet abnormalities, vasular disease. prolonged by asprin measuring function of factor VIII | Bleeding time |
| This test's function is a test of platelet adhesion, aggregation, and secretion. detects qualitative platelet defects | Platelet aggregation |
| 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) |
| this test detects deficiencies in the intrinsic and common pathways, most common test to monitor heparin therapy | Activated partial throboplastin time (APTT) |
| this test is used very little to monitor heparin therapy (fibrinogen in common pathway) | Thrombin time (TT) |
| This test is a Factor XIII screening test | Urea solubility |
| this test is positive in DIC, Deep vein thrombosis, pulmonary embolism, and after lytic therapy, but negative in primary fibrinolysis | D-dimer |
| this is the precursor of plasmin, is decreased following lytic therapy, DIC, and primary fibrinolysis | plasminogen |
| Hepran cofactor, deficiencys associated with thrombosis | Antithrombin III |
| Inhibitors of coagulation deficiencies associated with thromboembolic disorders | Protein C and S |
| This deficiency has a normal PT, abnormal APTT, is corrected by absorbed plasma, not corrected with aged serum | Factor VIII |
| This deficiency has a normal PT, abnormal APTT is corrected by Aged serum, not corrected by adsorbed plasma | Factor IX |
| This deficiency has normal PT, abnormal APTT is corrected by both aged serum and absorbed plasma | XI |
| This deficiency has normal PT, abnormal APTT, and is corrected by aged serum and adsorbed plasma | factor XII |
| This deficiency has an abnormal PT and APTT, and is corrected by adsorbed plasma, not corrected by aged serum | factor I |
| This deficiency has an abnormal PT and APTT, and is not corrected by Aged serum and adsorbed plasma | Factor II |
| This deficiency has an abnormal PT and APTT and is corrected by adsorbed plasma, not corrected by aged serum | V |
| This deficiency has an abnormal PT and APTT and is corrected by aged serum, not corrected by adsorbed plasma | factor X |
| Adsorbed serum corrects which factors | V, VIII, XI, XII |
| Aged plasma corrects which factors | VII, IX, X, XI, XII |
| What disease is associated with the following findings Decreased Factor VIII APTT prolongs PT normal Bleeding time Normal Platelet count normal | Hemophilia A |
| What disease is associated with these lab findings APTT prolonged PT normal Bleeding time normal Platelet count normal | Hemophilia B |
| 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 |
| 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 |
| What disease is associated with these findings bleeding time prolonged giant platelets platelet cound decreased clot retraction normal | Bernard Soulier syndrome |
| What are the key differences in DIC and primary fibrinolysis | Platelets, D-Dimer, Antithrombin III, and RBC Morphology |
| 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 |
| 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 |
| 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 |
| What drugs are used in thrombolytic therapy | strptokinase, urokinase, tissue plasminogen activator, prourokinase, acylated plasminogen streptokinase actvated complex |
| What changes are induced by thrombolytic therapy | decrease in fibrinogen, plasminogen, V, VII, IX, XII increase in plasmin, FDP, D-dimer, APTT, PT, TT |
Created by:
jnwells03
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