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Hemostasis Exam 1
CH 37-39
| Question | Answer |
|---|---|
| Proteins C + S | aid in preventing excess clotting; deficiency --> thrombotic disorder |
| platelet adhesion --> platelet aggregation --> | VWF fibrinogen |
| plasma coag zymogens | serine proteases that form complexes to activate others to generate thrombin |
| what stabilizes the fibrin monomers to form a clot after thrombin cleaves fibrinogen? | FXIIIa |
| what does FVIII depend on for stability | VWF |
| oral anticoagulation is based on | vitamin K antagonism |
| vitamin K | promotes synthesis of II, VII, IX, and X |
| contact group | XII and prekallikrein |
| thrombin | comes from prothrombin forms thrombin-thrombomodulin complex to activate the protein C pathway suppresses coagulation by degrading FVa and FVIIIa initiates platelet aggregation activates FV, VIII, XIII |
| Heparin | binds to antithrombin to inhibit thrombin so a fibrinogen can't be cleaved and a clot can't be formed |
| what converts plasminogen to plasmin? | TPA/UPA |
| Cofactors | stabilize and increase activity |
| what is FXIIIa important for? | stabilizing the clot |
| Aspirin | inactivates cyclooxygenase causing impairment in PLT function |
| what activates primary hemostasis? | Tissue injury and VWF |
| coagulation factors | the 16 procogulants found in plasma |
| which factors are serine proteases? | IIa, VIIa, IXa, XIa, XIIa, and PK |
| Disseminated Intravascular Coagulation (DIC) | thrombotic disorder that creates many tiny clots leading to generalized bleeding that can lead to shock or even death |
| warfarin/ coumadin | interferes with the gamma-carboxylation of prothrombin group proteins |
| Tissue factor forms a complex with _______ to activate _______ | VIIa; X |
| ______ and ______ promote FVIIa binding to tissue factor | VIIIa and Ca2+ |
| how can FXI be activated? | contact factor complex |
| How does XIIIa stabilize the fibrin clot? | By forming covalent bonds between the D-domains of the fibrin polymers |
| common pathway factors | I, II, V, X |
| intrinsic pathway factors | VIII, IX, XI, XII |
| extrinsic pathway factors | III and VII |
| where does TPA come from | damaged endothelial cells |
| what does recombinant TPA do in stroke patients? | dissolves clots |
| where does UPA come from | urine |
| what does purified urokinase preparations do | restore flow to intravenous catheters blocked by clotted blood/ fibrin |
| PAI-1 | Plasminogen activator 1 |
| alpha2-antiplasmin | inhibits plasmin to prevent/decrease fibrinolysis |
| how are D dimer concentrations assayed? | monoclonal antibody to the fragment using agglutination, chromatography, ELISA or latex immunoassay methos |
| elevated D dimers | thrombotic event has occurred |
| localized vs generalized | bleeding in one place vs bleeding in multiple places |
| mucocutaneous vs anatomic | in skin vs from trauma/procedures |
| congenital vs acquired | spontaneous vs from disease/disorder/deficiency |
| initial hemostasis profile | PT, PTT, PLT count |
| ________ is decreased and ___________ increased in DIC | fibrinogen; split products |
| unusual lab finding in sepsis induced DIC | increased fibrinogen (acute phase reactant) |
| what is the primary cause for bleeding in patients with renal failure? | Platelet dysfunction |
| what type of VWD is most common? | type 1 |
| type 1 VWD gives | normal PT, prolonged PTT, decreased FVII activity and increased PLT count |
| how is type 1 VWD treated | desmopressin acetate (DDAVP) |
| hemophilia all has | prolonged PTT and normal PT |
| what is used to screen for liver disease | PT |
| urea solubility test detects | FXIII deficiency |
| what factor distinguished liver disease from vitamin k deficiency | FV |
| if a patient's PTT doesn't rise after a typical heparin dose, run a | chromogenic antithrombin test |
| how to prevent skin necrosis during thrombin treatment? | use heparin in conjunction with warfarin for the first five days |
| patients receiving therapeutic heparin should regularly have what tested? | PTT and PLT count |
| what does FV leiden mutation do? | makes FV resistant to degradation by protein C |
| chromogenic assay for antithrombin | color intensity is directly proportional to concentration |
| what is used to activate protein C in the chromogenic assay? | snake venom |
| why must the tube drawn for PT/PTT be full? | so the 9:1 ratio is correct |
| what is bleeding time useful for? | PLT plug formation and capillary integrity |
| what bleeding time test method is easiest? which is the method of choice? | duke surgicutt |
| what other tests are used in conjunction with bleeding time? | PT, PTT, PLT count, Fbg, FDP, and PFA |
| what is clotting time test used for? | to monitor heparin therapy, assess coagulation status |
| hemostatic abnormalities | excessive clotting or excessive bleeding |
| FI | fibrinogen |
| FII | prothrombin |
| FIII | tissue factor |
| FIV | calcium |
| V | proaccelerin |
| VII | proconvertin |
| VIII | antihemophiliac factor A |
| IX | antihemophiliac factor B |
| X | stuart prower factor |
| XI | plasma |
| XII | Hageman |
| XIII | fibrin stabilizing factor |
| factor X deficiency | prolonged PT and PTT, normal TT |
| factor VII deficiency | prolonged PT, normal PTT and TT |
| factor VIII deficiency | prolonged PTT, normal PT and TT |
| fibrinogen deficiency | prolonged PTT, PT and TT |
| factor V deficiency | prolonged PT and PTT |
| intrinsic complex | IXa + VIII + PL + Calcium |
| prothrombinase complex | Xa + V PL + Calcium |
| extrinsic complex | TF Calcium + FVIIa |
| PTT | partial prothrombin time intrinsic 25-37 sec ref range |
| PT | Prothrombin time extrinsic 11-15 seconds ref range |
| TT | thrombin time 15-21 ref range |
Created by:
kingsleya27