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 |