Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Hemostasis Physiology: Characteristics of coagulation proteins: Contact protein, prothrombin protein, Fibrinogen protein Contact proteins: Prothrombin proteins: Fibrinogen proteins: - Factors: XII, XI, PK - Factors: II, VII, IX, X - Factors: I, V, VIII, XIII (prekallikrein) - Vit K dependent - Consumed during clotting (so, - Participates in initial phase of - NOT consumed during not in serum) intrinsic system clotting (except II) - Elevated in acute phase - NOT consumed during clotting (pregnancy & inflammation) (so found in serum & plasma) - NOT Vit K dependent Vasoconstriction is caused by several regulatory molecules which include: thromboxane A2 and serotonin Warfarin is classified as a Vit K antagonist. Factors that are impacted by warfarin therapy are: II, VII, IX, X A patient is placed on warfarin therapy, first factor that will be decreased: VII (proconvertin) Pt with family history of bleeding presents to the ED with aPPT normal; PT elevated pt on any medication; the factor likely to be deficient: VII Hageman factor (XII) is involved in all of these reactions except: transformation of fibrinogen to fibrin Most potent plasminogen activator in the contact phase of coagulation: Kallikrein The activation of plasminogen to plasmin resulting in the degradation of fibrin occurs by: tPA How does tissue factor pathway inhibitor inhibit coagulation: inhibition of tissue factor-factor VIIafactor Xa complex An inhibitor of plasmin activity is: alpha-2 antiplasmin Anti-thrombin inhibits factors: IIa and Xa The propagation phase of the in vivo coagulation model includes: a final burst of thrombin In the cell-based model of coagulation the intrinsic pathway operates on the: activated platelet surface to produce burst of thrombin A new oral anticoagulant apixaban has been given to a patient who was previously on warfarin. This drugs directly inhibits: Xa The anticoagulant that directly inhibits thrombin: argatroban A pt who presents with renal impairment is being started on oral anticoagulant therapy. The DOAC that should be avoided would be: dabigatran In secondary hemostasis, coagulation proteins become activated to from a fibrin clot. Prior to these proteins being activated, the inactive proenzymes are known as: zymogens Diseases or Disorders: Acquired disorder Inherited disorder Inhibitors Hemophilia A - pt with lupus anticoagulant may bleed due to: - Deficiency factor VIII antibodies to prothrombin - factor VIII pt with spontaneous bleeding: <1% - Most common coagulation factor in which - treat with commercial factor VIII specific inhibitor can form: VIII - Congenital hemophilia: found in - Anti-Factor VIII inhibitor: Only seen in Alloantibodies abnormal aPTT - A factor (X) assay done for dilutions if not agreeing within 10% the problem: Inhibitor Vit K deficiency: Hemophilia B - Deficiency factor IX - Factors: II, VII, IX, X - Decrease IX associated sex-linked 2 factors that differentiate vit K def & liver recessive disorder disease: V and VII - Problem with vit K deficiency: pt with celiac disease presents occult positive stools - Chronic ear infections; decreased vit K factors or: IX, II - Amyloidosis associated factor X Liver disease: Von willebrand disease - factors produce in the liver (II, V, VII, IX, X) - abnormal all aPTT, PLT screen, ristocetin cofactor (vWF activity) - Liver disease pt will present DECREASE factors - type III vWD: factor VIII level 2%, vWF activity (II, V, VII, IX, X) and vit k factors <1% with vWF antigen of 3% - 2 factors that differentiate vit K def & liver disease: V and VII Disseminated Intravascular Coagulation (DIC): Factor XIII deficiency - seen in unregulated and excessive formation - pt presents with bleeding 48 hrs after tooth of thrombin & plasmin extraction most - characterized by: Hypofibrinogenemia - common presentation: delayed bleeding - Tests prolonged PT, aPTT; decreased tendency fibrinogen, PLT count; increase D-dimers; on - if pt has factor XIII def; detect with: clot blood smear: schistocytes solubility in 5 molar urea solution (5M urea - none of the above; No single test specific test) for DIC, but combination of tests Lab Tests: Specimen collection/handing Sodium citrate for both (coag test & PLT aggregation studies) Routine tests for Hemostatic function Prothrombin Time (PT) Activated Partial Thromboplastin Time (aPTT) Fibrinogen Assay Thrombin Time (TT) Bleeding Time Platelet Function Assay (PFA test) Clot Retraction Factor Assays Dilute Russell’s Viper Venom test (DRVVT) Anti-factor Xa Assay Reptilase time Fibrinolysis testing