Explore key aspects of hematology in 'Meisenberg ch 15, plasma proteins' quiz, focusing on plasma proteins and their roles in blood coagulation. Assess your understanding of conditions like von Willebrand disease, the use of anticoagulants, and the biochemical properties of clotting factors.
Adhesion of platelets to the extracellular matrix
The synthesis of g-carboxyglutamate containing clotting factors
Contact phase activation
The extrinsic pathway of blood clotting
The cleavage of prothrombin to thrombin
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Warfarin can be used, but heparin cannot
Heparin can be used, but warfarin cannot
Both can be used
Neither can be used
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Increase the substrate specificity of the clotting factors, thereby preventing the incidental cleavage of other proteins
Bind the clotting factors to exposed components of the extracellular matrix
Serve as a feedback mechanism that makes the activated clotting factors sensitive to protease inhibitors
Create cleavage sites for proteolytic activations during zymogen processing
Bind the clotting factors to activated platelets
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Internal bleeding
Cholestatic jaundice
A pre-hepatic jaundice
Viral hepatitis
Gilbert's syndrome
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Factor V
Factor VIII
Factor IX
High-molecular-weight kininogen
Von Willebrand factor
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Platelet aggregation
Secretion of prostaglandins from endothelial cells
Secretion of thrombin from leukocytes
Formation of fibrin monomer
Contact phase activation
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Binding to fibrinogen and thereby preventing its cleavage by thrombin
Activating tissue-type plasminogen activator
Inhibiting urokinase
Inhibiting the binding of prothrombin to activated platelets
Activating antithrombin III
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Coumarin and related drugs activate the fibrinolytic system, in addition to blocking the clotting cascade
Only the intrinsic pathway of blood clotting is blocked in hemophilia, but intrinsic, extrinsic and final common pathways are all blocked in coumarin poisoning
Von Willebrand factor is abnormal in coumarin poisoning but not in classical hemophilia
Coumarin and related drugs inhibit contact phase activation in the intrinsic pathway; this process is intact in classical hemophilia
Fibrinogen is normal in classical hemophilia, but coumarin and related drugs cause the formation of structurally abnormal fibrinogen
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Y-globulins
A1-antiprotease
Ceruloplasmin
Fibrinogen
Haptoglobin
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Haptoglobin
Ferritin
Transferrin
α1-antiprotease
Hemoglobin
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Creatine kinase-MM
Alkaline phosphatase
Lactate dehydrogenase
Creatine kinase-MB
Alanine transaminase
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25 7.7
15 7.6
45 7.5
55 7.4
65 7.3
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Aspartate transaminase
Alkaline phosphatase
Amylase
γ-glutamyltransferase
Creatine kinase
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Tell the mother that the child is going to die in a few hours
Inject a high dose of tissue-type plasminogen activator, then keep monitoring the prothrombin time over the next days
Make an exchange transfusion immediately, then keep monitoring the activated partial thromboplastin time over the next days
Transfuse fresh frozen plasma immediately, to replace the defective clotting factors
Gastric lavage and injection of a high dose of vitamin K, and keep monitoring the prothrombin time over the next days
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Bence-Jones protein
Hypergammaglobulinemia
Waldenstrom's macroglobulinemia
Agammaglobulinemia
High levels of IgM
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Creatine kinase
Alkaline phosphatase
Lactate dehydrogenase
Cholinesterase
Amylase
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The plasma level of von Willebrand factor is reduced to 10% of normal
Injected heparin has a paradoxical pro-coagulant effect
The amino acid hydrolysate of a plasma sample contains an abnormally large quantity of y-carboxyglutamate
The boy’s blood clots when mixed with the blood of a patient with hemophilia A, but not when mixed with blood from a patient with hemophilia B
The prothrombin time is normal, but the activated partial thromboplastin time is greatly reduced
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IgM
IgG
IgA
IgD
IgE
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Thromboplastin
Thrombomodulin
Heparin
Vitamin K
Urokinase
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