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Phils Hemo Coag

QuestionAnswer
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