Question 1

Which autosomal dominant thrombotic disorder may present with deep venous thrombosis complicated by pulmonary embolism?

Accepted Answer

A)  Activated protein C resistance 
B)  Antithrombin III (AT-III) deficiency 
C)  Protein C deficiency 
D)  Protein S deficiency 
E)  All of the above 
A)  Activated protein C resistance 
B)  Antithrombin III (AT-III) deficiency 
C)  Protein C deficiency 
D)  Protein S deficiency 
E)  All of the above

Question 2

Streptokinase and urokinase are __________ plasminogen activators.

Accepted Answer

A)  Fibrin specific 
B)  Non-fibrin-specific 
C)  Thrombin nonspecific 
D)  Thrombin specific 
E)  None of the above 
A)  Fibrin specific 
B)  Non-fibrin-specific 
C)  Thrombin nonspecific 
D)  Thrombin specific 
E)  None of the above

Question 3

Protein S is a vitamin K-dependent protein that is produced in the __________.

Accepted Answer

A)  Liver 
B)  Megakaryocytes 
C)  Endothelial cells 
D)  All of the above 
E)  None of the above 
A)  Liver 
B)  Megakaryocytes 
C)  Endothelial cells 
D)  All of the above 
E)  None of the above

Question 4

Which autosomal dominant thrombotic disorder is associated with an increased risk of warfarin-induced skin necrosis?

Accepted Answer

A)  Protein C deficiency 
B)  Protein S deficiency 
C)  Antithrombin deficiency 
D)  A and B 
E)  All of the above 
A)  Protein C deficiency 
B)  Protein S deficiency 
C)  Antithrombin deficiency 
D)  A and B 
E)  All of the above

Question 5

In trying to explain a prolonged APTT, the following should be considered:

Accepted Answer

A)  The possibility that there is heparin in the specimen 
B)  Hypofibrinogenemia and/or DIC 
C)  Elevated hematocrit resulting in too much anticoagulant in the tube for the amount of plasma present and/or traumatic venipuncture 
D)  Specific factor deficiency or an inhibitor 
E)  All of the above 
A)  The possibility that there is heparin in the specimen 
B)  Hypofibrinogenemia and/or DIC 
C)  Elevated hematocrit resulting in too much anticoagulant in the tube for the amount of plasma present and/or traumatic venipuncture 
D)  Specific factor deficiency or an inhibitor 
E)  All of the above

Question 6

Protein C function is significantly increased in the presence of:

Accepted Answer

A)  Calcium 
B)  Protein S 
C)  Phospholipids 
D)  A and B 
E)  B and C 
A)  Calcium 
B)  Protein S 
C)  Phospholipids 
D)  A and B 
E)  B and C

Question 7

Clinical manifestations of heterozygous AT-III deficiency (such as thrombotic episodes before age 40) may occur in association with:

Accepted Answer

A)  Surgery 
B)  Pregnancy 
C)  Oral contraceptives 
D)  Trauma 
E)  All of the above 
A)  Surgery 
B)  Pregnancy 
C)  Oral contraceptives 
D)  Trauma 
E)  All of the above

Question 8

The primary aim of thrombolytic therapy is to activate __________.

Accepted Answer

A)  Plasminogen into plasmin 
B)  Prothrombin into thrombin 
C)  Fibrinogen to fibrin 
D)  Factor VIII into hemophilia factor 
E)  Factor V into activated protein C 
A)  Plasminogen into plasmin 
B)  Prothrombin into thrombin 
C)  Fibrinogen to fibrin 
D)  Factor VIII into hemophilia factor 
E)  Factor V into activated protein C

Question 9

Which of the following statements about hyperhomocysteinemia is/are true?

Accepted Answer

A)  Hyperhomocysteinemia can be inherited or acquired. 
B)  Deficiencies of folate, vitamin B6, and vitamin B12 can cause hyperhomocysteinemia. 
C)  Mutation in the methylene tetrahydrofolate reductase (MTHFR) gene is responsible for some forms of hyperhomocysteinemia. 
D)  Mild to moderate hyperhomocysteinemia is an independent risk factor for arterial thrombotic diseases such as stroke, myocardial infarction, and peripheral vascular disease. 
E)  All of the above 
A)  Hyperhomocysteinemia can be inherited or acquired. 
B)  Deficiencies of folate, vitamin B6, and vitamin B12 can cause hyperhomocysteinemia. 
C)  Mutation in the methylene tetrahydrofolate reductase (MTHFR) gene is responsible for some forms of hyperhomocysteinemia. 
D)  Mild to moderate hyperhomocysteinemia is an independent risk factor for arterial thrombotic diseases such as stroke, myocardial infarction, and peripheral vascular disease. 
E)  All of the above

Question 10

All of the following influence clot formation except:

Accepted Answer

A)  Characteristics of the vessel wall (especially the endothelium) 
B)  Turbulence of blood flow 
C)  Procoagulant and anticoagulant factors in the blood 
D)  Speed of blood flow 
E)  Height 
A)  Characteristics of the vessel wall (especially the endothelium) 
B)  Turbulence of blood flow 
C)  Procoagulant and anticoagulant factors in the blood 
D)  Speed of blood flow 
E)  Height

Question 11

Which of the following is NOT among the standard criteria for aPL syndrome?

Accepted Answer

A)  Arterial thrombosis 
B)  Venous thrombosis 
C)  The patient must have systemic lupus erythematosus 
D)  Certain patterns of pregnancy loss 
E)  LA or medium to high aCL titer on at least two occasions at least 6 weeks apart 
A)  Arterial thrombosis 
B)  Venous thrombosis 
C)  The patient must have systemic lupus erythematosus 
D)  Certain patterns of pregnancy loss 
E)  LA or medium to high aCL titer on at least two occasions at least 6 weeks apart

Question 12

The central reaction in the fibrinolytic system is the conversion of:

Accepted Answer

A)  Fibrinogen to fibrin 
B)  Prothrombin to thrombin 
C)  Plasminogen to plasmin 
D)  Plasmin to plasminogen 
E)  None of the above 
A)  Fibrinogen to fibrin 
B)  Prothrombin to thrombin 
C)  Plasminogen to plasmin 
D)  Plasmin to plasminogen 
E)  None of the above

Question 13

Which form of protein S functions as the cofactor for protein C?

Accepted Answer

A)  Free form 
B)  C4BbP bound 
C)  C5 convertase bound 
D)  C3 convertase bound 
E)  None of the above 
A)  Free form 
B)  C4BbP bound 
C)  C5 convertase bound 
D)  C3 convertase bound 
E)  None of the above

Question 14

Why is thrombogenesis greatly accelerated by the presence of platelets?

Accepted Answer

A)  The phospholipid platelet membrane offers support for the surface-dependent activation process of coagulation. 
B)  Thrombin can stimulate the platelet release reaction. 
C)  Alpha granules contain, among other things, fibrinogen, factor V, and von Willebrand's factor (vWF) 
D)  All of the above 
E)  None of the above 
A)  The phospholipid platelet membrane offers support for the surface-dependent activation process of coagulation. 
B)  Thrombin can stimulate the platelet release reaction. 
C)  Alpha granules contain, among other things, fibrinogen, factor V, and von Willebrand's factor (vWF) 
D)  All of the above 
E)  None of the above

Question 15

Regarding laboratory testing to detect known causes of thrombosis:

Accepted Answer

A)  Testing is best performed as soon as possible after the thrombosis is diagnosed, but before the patient receives anticoagulants. 
B)  It is best to test using plasma drawn after the patient has begun anticoagulant therapy, so the effects of the thrombus are masked. 
C)  Testing during the acute thrombotic event can result in false positives and false negatives 
D)  Genetically based tests, such as those for MTHFR, prothrombin G20210A, and factor V Leiden, are affected by anticoagulant therapy and the presence of thrombus. 
E)  It is acceptable to test for inherited causes of thrombophilia during the acute event, but not for acquired causes. 
A)  Testing is best performed as soon as possible after the thrombosis is diagnosed, but before the patient receives anticoagulants. 
B)  It is best to test using plasma drawn after the patient has begun anticoagulant therapy, so the effects of the thrombus are masked. 
C)  Testing during the acute thrombotic event can result in false positives and false negatives 
D)  Genetically based tests, such as those for MTHFR, prothrombin G20210A, and factor V Leiden, are affected by anticoagulant therapy and the presence of thrombus. 
E)  It is acceptable to test for inherited causes of thrombophilia during the acute event, but not for acquired causes.

Question 16

How is a deficiency of protein S different from other vitamin K-dependent plasma protein deficiencies?

Accepted Answer

A)  Deficiency may involve abnormality of the protein S antigen. 
B)  The quantitative distribution of protein S between free and bound forms may contribute to functional deficiency. 
C)  Deficiency may involve abnormally low levels of protein S. 
D)  All of the above 
E)  None of the above 
A)  Deficiency may involve abnormality of the protein S antigen. 
B)  The quantitative distribution of protein S between free and bound forms may contribute to functional deficiency. 
C)  Deficiency may involve abnormally low levels of protein S. 
D)  All of the above 
E)  None of the above

Question 17

The APTT-based screening test for APC-R involves:

Accepted Answer

A)  Using reagent plasma with excess factor V 
B)  Diluting patient plasma with factor V-deficient plasma 
C)  Making a ratio of two clotting times, one with added APC and one without 
D)  A and B 
E)  B and C 
A)  Using reagent plasma with excess factor V 
B)  Diluting patient plasma with factor V-deficient plasma 
C)  Making a ratio of two clotting times, one with added APC and one without 
D)  A and B 
E)  B and C

Question 18

The quantity of __________ present regulates the rate of formation of activated protein C.

Accepted Answer

A)  XIIIa 
B)  Va 
C)  IIIa 
D)  VIIIa 
E)  IXa 
A)  XIIIa 
B)  Va 
C)  IIIa 
D)  VIIIa 
E)  IXa

Question 19

Which of the following is true about heparin-induced thrombocytopenia (HIT)?

Accepted Answer

A)  It is heralded by a sudden unexplained decrease in platelets on the first day of heparin therapy. 
B)  Because HIT patients are thrombocytopenic, they are all at high risk for bleeding complications. 
C)  It appears to be caused by an immune response related to heparin exposure. 
D)  If a patient did not develop HIT the first time he or she was ever exposed to heparin, then he or she has no risk of developing HIT on subsequent exposures to heparin. 
E)  All of the above 
A)  It is heralded by a sudden unexplained decrease in platelets on the first day of heparin therapy. 
B)  Because HIT patients are thrombocytopenic, they are all at high risk for bleeding complications. 
C)  It appears to be caused by an immune response related to heparin exposure. 
D)  If a patient did not develop HIT the first time he or she was ever exposed to heparin, then he or she has no risk of developing HIT on subsequent exposures to heparin. 
E)  All of the above

Question 20

Which statement about lupus anticoagulants (LAs) and antiphospholipid (aPL) syndrome is true?

Accepted Answer

A)  LAs are best detected by enzyme-linked immunosorbent assay (ELIS
A)  for anticardiolipin (aCL) antibodies. 
B)  All prolongations of the APTT are caused by LAs. 
C)  The presence of either a positive ELISA for aCL or an LA is sufficient to label a patient as having aPL syndrome. 
D)  aPL syndrome is associated only with arterial thrombosis. 
E)  The term "LA" is inherently confusing, because although LAs prolong coagulation tests, they are known for their association with thrombotic disease, not bleeding. 
A)  LAs are best detected by enzyme-linked immunosorbent assay (ELIS
A)  for anticardiolipin (aCL) antibodies. 
B)  All prolongations of the APTT are caused by LAs. 
C)  The presence of either a positive ELISA for aCL or an LA is sufficient to label a patient as having aPL syndrome. 
D)  aPL syndrome is associated only with arterial thrombosis. 
E)  The term "LA" is inherently confusing, because although LAs prolong coagulation tests, they are known for their association with thrombotic disease, not bleeding.

Exam 28: Introduction to Thrombosis and Anticoagulant Therapy

Which autosomal dominant thrombotic disorder may present with deep venous thrombosis complicated by pulmonary embolism?

Streptokinase and urokinase are __________ plasminogen activators.

Protein S is a vitamin K-dependent protein that is produced in the __________.

Which autosomal dominant thrombotic disorder is associated with an increased risk of warfarin-induced skin necrosis?

In trying to explain a prolonged APTT, the following should be considered:

Protein C function is significantly increased in the presence of:

Clinical manifestations of heterozygous AT-III deficiency (such as thrombotic episodes before age 40) may occur in association with:

The primary aim of thrombolytic therapy is to activate __________.

Which of the following statements about hyperhomocysteinemia is/are true?

All of the following influence clot formation except:

Which of the following is NOT among the standard criteria for aPL syndrome?

The central reaction in the fibrinolytic system is the conversion of:

Which form of protein S functions as the cofactor for protein C?

Why is thrombogenesis greatly accelerated by the presence of platelets?

Regarding laboratory testing to detect known causes of thrombosis:

How is a deficiency of protein S different from other vitamin K-dependent plasma protein deficiencies?

The APTT-based screening test for APC-R involves:

The quantity of __________ present regulates the rate of formation of activated protein C.

Which of the following is true about heparin-induced thrombocytopenia (HIT)?

Which statement about lupus anticoagulants (LAs) and antiphospholipid (aPL) syndrome is true?

Morphology of Human Blood and Marrow Cells: Hematopoiesis

Bone Marrow

The Red Blood Cell: Structure and Function

Anemia: Diagnosis and Clinical Considerations

Evaluation of Red Blood Cell Morphology and Introduction to Platelet and White Blood Cell Morphology

Iron Metabolism and Hypochromic Anemias

Megaloblastic Anemias

Aplastic Anemia Including Pure Red Cell Aplasia and Congenital Dyserythropoietic Anemia and Paroxysmal Nocturnal Hemoglobinuria

Introduction to Hemolytic Anemias: Intracorpuscular Defects: I Hereditary Defects of the Red Cell Membrane

Hemolytic Anemias: Intracorpuscular Defects: II Hereditary Enzyme Deficiencies

Hemolytic Anemias: Intracorpuscular Defects: III the Hemoglobinopathies

Hemolytic Anemias: Intracorpuscular Defects: Iv Thalassemia

Hemolytic Anemias: Extracorpuscular Defects

Hypoproliferative Anemia: Anemia Associated With Systemic Diseases

Cell Biology, Disorders of Neutrophils, Infectious Mononucleosis, and Reactive Lymphocytosis

Introduction to Leukemia and the Acute Leukemias

Chronic Myeloproliferative Disorders I: Chronic Myelogenous Leukemia

Chronic Myeloproliferative Disorders Ii: Polycythemia Vera, Essential Thrombocythemia, and Idiopathic Myelofibrosis

Myelodysplastic Syndromes

Chronic Lymphocytic Leukemia and Related Lymphoproliferative Disorders

The Lymphomas

Multiple Myeloma and Related Plasma Cell Disorders

Lipid Lysosomal Storage Diseases and Histiocytosis

Introduction to Hemostasis

Disorders of Primary Hemostasis: Quantitative and Qualitative Platelet Disorders and Vascular Disorders

Disorders of Plasma Clotting Factors

Interaction of the Fibrinolytic, Coagulation, and Kinin Systems; Disseminated Intravascular Coagulation; and Related Pathology

Quality Control in the Hematology Laboratory

Body Fluid Examination: the Qualitative, Quantitative, and Morphologic Analysis of Serous, Cerebrospinal, and Synovial Fluids

Hematology Methods

Principles of Automated Differential Analysis

Coagulation Procedures

Applications of Flow Cytometry to Hematology and Hemostasis

Molecular Diagnostic Techniques in Hematopathology

Special Stainscytochemistry

Filters