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50 Cards in this Set
- Front
- Back
What are the 4 steps to primary hemostasis?
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1 - initiated by vascular injury
2 - platelet adhesion to damaged endothelium 3- platelet aggregation --> activation of intrinsic clotting 4 - platelet thrombus |
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What is the goal of secondary hemostasis?
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stabilizes the platelet thrombus by formation of a fibrin network
-extrinsitc, intrinsic, common pathways |
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What pathway is the most important?
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extrinsic (factor 7)
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What is factor 7 activated by?
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tissue thromboplastin (factor)
-this is released from damaged vascular cells |
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What does activated factor 7 do?
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activates factor 10 of the common pathway
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What are factors 12, 11, 9, 8 activated by?
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collagen (exposed by vascular damage) phospholipid, and other substances
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What does factor 8 do once activated?
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activated factor 10
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Which factors convert prothrombin to thrombin?
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10 and 5
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What is the final step of secondary hemostasis?
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conversion of fibrinogen to fibrin using factor 2
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What are the inhibitors of coagulation?
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protein C,
antithrombin III, tissue factor pathway inhibitor - 1, protein S, plasmin |
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What must he platelet count be to cause hemorrhage?
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50,000 or below
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What are the pirmary coagulopathies?
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thrombocytopenia, thrombocytopathic
endothelial disease |
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What are petechia most often associated with?
ecchymosis? |
abnormal primary hemostasis
abnormal secondary hemostasis (coagulopathy) |
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What is epistaxis most commonly associated with?
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primary hemostasis
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What does Buccal mucosal bleeding time measure?
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platelet and endothelial function --> prolonged by any one of the problems that cause primary coagulopathies
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What does prothrombin time test?
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extrinsic and common pathways
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WIth Vitamin K def., what increases first?
What about with heparin? |
PT before PTT
PTT before PT |
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What is ACT?
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time for visible clot to form
-tests intrinsic and common pathways |
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Why might fibrinogen be decreased?
increased? |
-decreased production by liver or increased consuption (DIC)
inflammation |
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What are FDPs formed by?
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break down of fibriongen and fibrin (fibrinolysis)
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What do elevated FDPs infer?
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excessive coagulation with subsequent fibrionlysis as in DIC
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What do D-dimers measure?
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fibrin degradation products
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When is AT III decreased?
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in DIC, neprhotic syndrome
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What are the 4 main causes of thrombocytopenia?
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1 - destruction
2 - consumption 3 - sequestration 4 - decreaed production |
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What are 2 reasons why platelets may be destroyed?
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1 - immune-mediated (primary or secondary (to neoplasia, infection, drugs)
2 - infectious |
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What are 3 reasons why platelets may be consumed?
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1 - DIC
2 - vasculitis (rickettsial infections, FIP, immune-mediated) 3 - severe acute hemorrhage |
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Why would platelets be sequestered?
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hyperspenism
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What are 7 reasons why platelets would stop being produced?
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1 - marrow neoplasia
2 - immune-mediated 3 - infection (Ehrlichia, FeLV) 4 - drugs 5 - estrogen 6 - myelofibrosis 7 - myelodysplasia |
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What test would you want to perform if you have thrombocytopenia and have already done a PE, CBC, chemistry, and UA?
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serological tests for: Babesia, RMSF,
Ehrlichia, FeLV, FIV -rads -antinuclear antibodies (for immune-mediated disease) |
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What things (3) may cause secondary IMTP?
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- infection: Ehrlichia and RMSF
-vaccination (3-10 days post) - drugs (sulfonamides) |
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What is seen on a CBC with IMTP?
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-severe thrombocytopenia (<40,000 and often less than 10,000)
-anemia (due to bleeding) - neutrophilia |
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What is Evan's Syndrome?
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Concurrent IMTP and immune-mediated hemolytic anemia
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What concurrent diseases should you look for with IMTP?
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neoplasia
infection (RMSF, Ehrilichia, HW, sepsis, viral DIC Drugs/vaccinnation history |
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What is the treatment for IMTP?
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1 - cage rest
2 - platelet transfusion 3 - Immunosuppression (gluococorticoids) |
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How should you taper the prednisone dose when treating IMTP?
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- taper by 25-33% every 2-4 weeks after platelet count goes back to normal
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What are common clinical findings in animals with von Willebrands Disease?
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- hemorrhage following trauma or surgery
-mucosal bleeding - epistaxis or urogenital |
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How do you diagnose von Willebrand's disease?
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- vWf:ag
-buccal mucosal bleeding time - genetic test |
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What is the most effective treatment for von Willebrand's disease?
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cryoprecipitate
-desmopressin causes release of vWF from endothelium |
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What is the difference between warfarin and second gen vit. K antagonists such as brodifacoum, dipheacinon?
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duration of action
warfarin - short acting with duration 10-14 d sec gen - duration of action 3-4 weeks |
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What are the vit k dep. coagulation factors?
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2,7,9,10
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Why is PT increased before PTT with vit. K antagonists?
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factor 7 has the shortest half-life (6 hours)
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What is the treatment for vit. k antagonists?
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Vitamin K1
-oral initially if not showing CS -SQ initial if showing CS followed by oral - with plasma or whole blood -RBC -IV fluids -thoracocentisis |
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What are 4 acquired coagulation factor def?
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1 - vitamin K antagonist
2 - liver disease 3 - neoplasia 4 - DIC |
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What are the results of hepatic failure?
- must be severe |
1 - factor def. (coag)
2 - def. of vitamin K (due to cholestasis with anorexia) |
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What is very important in perpetuating DIC?
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antithrombin III deficiency
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What are the CS associated with chronic compensated DIC?
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none
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What are CS associated with acute decompensated DIC?
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- hemorrhage
-shock (hemorrhage due to using up coagulation factors and hypotension) - organ failure -thrombosis of any organ |
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What are common this used to diagnose DIC?
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1 - prolonged PT and PTT
2 - thrombocytopenia 3 -increased FDP and D-dimer 4 - decreased fibrinogen - due to fibrinolysis 5 -decreased AT - III 6 -schistocytes |
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What is the best treatment for DIC?
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resolution of the primary problem
-also IV fluids -oxygen -plasma transfusion -anticoagulant treatment - heparin (low doses) |
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What does low dose heparin do for DIC patients?
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- activates AT III, making it more potent
-acts on AT III to inactivate factor Xa |