Question 1

Antithrombin and heparin cofactor II primarily inhibit which of the following factors?

Accepted Answer

A) F-V, F-VIII, and thrombin 
B) F-IXa, F-Xa, and thrombin 
C) F-XII and thrombin 
D) Fibrinogen and thrombin 
A) F-V, F-VIII, and thrombin 
B) F-IXa, F-Xa, and thrombin 
C) F-XII and thrombin 
D) Fibrinogen and thrombin B

Question 2

Which of the following mechanisms can lead to an increased risk of thrombosis?

Accepted Answer

A) Increased concentration of plasminogen activator 
B) Deficiency of plasminogen 
C) Deficiency of plasminogen activator inhibitor 
D) Increased concentration of plasminogen 
A) Increased concentration of plasminogen activator 
B) Deficiency of plasminogen 
C) Deficiency of plasminogen activator inhibitor 
D) Increased concentration of plasminogen B

Question 3

How does heparin inhibit coagulation?

Accepted Answer

A) It chelates calcium release from platelet granules. 
B) It catalyzes antithrombin activity. 
C) It neutralizes labile factors V and VIII. 
D) It neutralizes the tenase complex. 
A) It chelates calcium release from platelet granules. 
B) It catalyzes antithrombin activity. 
C) It neutralizes labile factors V and VIII. 
D) It neutralizes the tenase complex. B

Question 4

Which of the following best describes the most common cause of hyperhomocysteinemia?

Accepted Answer

A) Mutations in the CBS gene or MTHFR gene 
B) APCR 
C) TFPI variant 
D) Substitution in the 3' untranslated region of the prothrombin gene (nucleotide 20210) 
A) Mutations in the CBS gene or MTHFR gene 
B) APCR 
C) TFPI variant 
D) Substitution in the 3' untranslated region of the prothrombin gene (nucleotide 20210)

Question 5

During coumadin-induced anticoagulation, which factor's activity disappears most rapidly?

Accepted Answer

A) F-IX 
B) F-VII 
C) F-VIII 
D) F-V 
A) F-IX 
B) F-VII 
C) F-VIII 
D) F-V

Question 6

Name the genetic mutation that induces increased concentration of prothrombin in the circulation that leads to increased risk of venous thrombosis.

Accepted Answer

A) G → A substitution on nucleotide 20210 of the prothrombin gene 
B) Lysine to glutamic acid substitution on the sixth position on the beta globin chain 
C) Arginine to glutamine substitution at the 506 position of prothrombin 
D) Translocation of chromosome 22 onto the long arm of chromosome 9 
A) G → A substitution on nucleotide 20210 of the prothrombin gene 
B) Lysine to glutamic acid substitution on the sixth position on the beta globin chain 
C) Arginine to glutamine substitution at the 506 position of prothrombin 
D) Translocation of chromosome 22 onto the long arm of chromosome 9

Question 7

How do red thrombi differ from white thrombi?

Accepted Answer

A) Their location 
B) Their composition 
C) Their location and composition 
D) Their degree of severity 
A) Their location 
B) Their composition 
C) Their location and composition 
D) Their degree of severity

Question 8

A patient has been taking coumadin for a recent thrombophilic episode.He follows up with his physician two weeks after he started this treatment.The physician sees evidence of skin necrosis on the patient.What should the physician do next to investigate this finding?

Accepted Answer

A) Draw and request a PT and an APTT 
B) Draw and request a PC antigen assay 
C) Draw and request a HC-II antigen assay 
D) Draw and request a PS antigen assay 
A) Draw and request a PT and an APTT 
B) Draw and request a PC antigen assay 
C) Draw and request a HC-II antigen assay 
D) Draw and request a PS antigen assay

Question 9

Why are clotting and molecular assays both needed for a diagnosis of APCR?

Accepted Answer

Because up to 10% of

Question 10

How does the INR standardize the prothrombin time?

Accepted Answer

The INR is calculated by taking the pati

Question 11

It has been determined that a patient has activated protein C resistance.Name the most prevalent genetic mutation associated with this finding.

Accepted Answer

A) Guanine to adenine substitution on nucleotide 20210 of the prothrombin gene 
B) Lysine to glutamic acid substitution on the sixth position on the beta globin chain 
C) Arginine to glutamine substitution at the 506 position of factor V protein 
D) Translocation of chromosome 22 onto the long arm of chromosome 9 
A) Guanine to adenine substitution on nucleotide 20210 of the prothrombin gene 
B) Lysine to glutamic acid substitution on the sixth position on the beta globin chain 
C) Arginine to glutamine substitution at the 506 position of factor V protein 
D) Translocation of chromosome 22 onto the long arm of chromosome 9

Question 12

Which laboratory test is considered to have a reliable negative predictive value in the diagnosis of DVT?

Accepted Answer

A) Factor VLeiden 
B) PT 
C) tPA 
D) D-dimer 
A) Factor VLeiden 
B) PT 
C) tPA 
D) D-dimer

Question 13

How do unfractionated heparin and low-molecular weight heparin differ?

Accepted Answer

A) In their pharmacokinetics 
B) In their composition 
C) In the tests used to monitor their biologic activity 
D) All of the above 
A) In their pharmacokinetics 
B) In their composition 
C) In the tests used to monitor their biologic activity 
D) All of the above

Question 14

Which of the following inherited condition is considered a low risk for a venous thromboembolic event?

Accepted Answer

A) Homozygous factor VLeiden 
B) Homozygous prothrombin 20210 
C) Homozygous AT, PC, or PS deficiency 
D) Sickle-cell anemia 
A) Homozygous factor VLeiden 
B) Homozygous prothrombin 20210 
C) Homozygous AT, PC, or PS deficiency 
D) Sickle-cell anemia

Question 15

Failure of protein C to destroy F-Va and F-VIIIa results in what hemostatic system alteration?

Accepted Answer

A) An increase in platelets 
B) An increase in production of thrombin 
C) An increase in F-VIII 
D) An increase in F-Xa 
A) An increase in platelets 
B) An increase in production of thrombin 
C) An increase in F-VIII 
D) An increase in F-Xa

Question 16

Antibodies to which component(s) are thought to complex with the phospholipids resulting in antiphospholipid antibody syndrome?

Accepted Answer

A) Homocysteine 
B) Fibrinogen and fibrin 
C) β2-glycoprotein-1, prothrombin, PC, PS, and F-VII 
D) Plasminogen and plasmin 
A) Homocysteine 
B) Fibrinogen and fibrin 
C) β2-glycoprotein-1, prothrombin, PC, PS, and F-VII 
D) Plasminogen and plasmin

Question 17

A patient with thrombophilia has a decreased functional and antigenic activity of protein C.What is the diagnosis?

Accepted Answer

A) APCR 
B) Protein S deficiency 
C) Type I PC deficiency 
D) Type II PC deficiency 
A) APCR 
B) Protein S deficiency 
C) Type I PC deficiency 
D) Type II PC deficiency

Question 18

Why does a patient who had a thrombotic incident receive both heparin and coumadin for 4-5 days before heparin is discontinued?

Accepted Answer

A) Heparin is not effective as an anticoagulant without Coumadin present. 
B) Coumadin requires heparin for its full anticoagulant effect. 
C) This gives the patient an initial bolus dose of anticoagulant. 
D) Coumadin 's full effect is not achieved for 4-5 days after initiation of this therapy due to the half life of the vitamin K coagulation factors. 
A) Heparin is not effective as an anticoagulant without Coumadin present. 
B) Coumadin requires heparin for its full anticoagulant effect. 
C) This gives the patient an initial bolus dose of anticoagulant. 
D) Coumadin 's full effect is not achieved for 4-5 days after initiation of this therapy due to the half life of the vitamin K coagulation factors.

Question 19

Patients with a DVT are at risk for developing which of the following?

Accepted Answer

A) Transient ischemic attacks 
B) Peripheral artery disease 
C) Myocardial infarction 
D) Pulmonary emboli 
A) Transient ischemic attacks 
B) Peripheral artery disease 
C) Myocardial infarction 
D) Pulmonary emboli

Question 20

How does a thrombus become a thromboembolus?

Accepted Answer

A thrombus is an initial formation of a

Exam 32: Thrombophilia

Antithrombin and heparin cofactor II primarily inhibit which of the following factors?

Which of the following mechanisms can lead to an increased risk of thrombosis?

How does heparin inhibit coagulation?

Which of the following best describes the most common cause of hyperhomocysteinemia?

During coumadin-induced anticoagulation, which factor's activity disappears most rapidly?

Name the genetic mutation that induces increased concentration of prothrombin in the circulation that leads to increased risk of venous thrombosis.

How do red thrombi differ from white thrombi?

A patient has been taking coumadin for a recent thrombophilic episode.He follows up with his physician two weeks after he started this treatment.The physician sees evidence of skin necrosis on the patient.What should the physician do next to investigate this finding?

Why are clotting and molecular assays both needed for a diagnosis of APCR?

How does the INR standardize the prothrombin time?

It has been determined that a patient has activated protein C resistance.Name the most prevalent genetic mutation associated with this finding.

Which laboratory test is considered to have a reliable negative predictive value in the diagnosis of DVT?

How do unfractionated heparin and low-molecular weight heparin differ?

Which of the following inherited condition is considered a low risk for a venous thromboembolic event?

Failure of protein C to destroy F-Va and F-VIIIa results in what hemostatic system alteration?

Antibodies to which component(s) are thought to complex with the phospholipids resulting in antiphospholipid antibody syndrome?

A patient with thrombophilia has a decreased functional and antigenic activity of protein C.What is the diagnosis?

Why does a patient who had a thrombotic incident receive both heparin and coumadin for 4-5 days before heparin is discontinued?

Patients with a DVT are at risk for developing which of the following?

How does a thrombus become a thromboembolus?

Introduction

Cellular Homeostasis

Hematopoiesis

Structure and Function of Hematopoietic Organs

The Erythrocyte

Hemoglobin

The Leukocyte

Introduction to Anemia

Anemias of Disordered Iron Metabolism and Heme Synthesis

Hemoglobinopaties: Qualitative Defects

Thalassemia

Megaloblastic and Nonmegaloblastic Macrocytic Anemias

Introduction to Hemolytic Anemia

Hemolytic Anemia: Membrane Defects

Hemolytic Anemia: Enzyme Deficiencies

Hemolytic Anemia: Immune Anemias

Hemolytic Anemia: Nonimmune Defects

Nonmalignant Granulocyte and Monocyte Disorders

Nonmalignant Lymphocyte Disorders

Introduction to Hematopoietic Neoplasms

Myeloproliferative Disorders

Myelodysplastic Syndromes

Acute Myeloid Leukemias

Acute Lymphoblastic Leukemias

Lymphoid Malignancies: Chronic Lymphoid Leukemias, Lymphomas, and Plasma Cell Neoplasms

Hematopoietic Stem Cell Transplantation

Morphologic Analysis of Body Fluids in the Hematology Laboratory

Primary Hemostasis

Secondary Hemostasis and Fibrinolysis

Disorders of Primary Hemostasis

Disorders of Secondary Hemostasis

Hematology Procedures and Hemostasis

Bone Marrow Examination

Automation in Hematology and Hemostasis

Flow Cytometry

Chromosome Analysis of Hematopoietic and Lymphoid Disorders

Molecular Analysis of Hematologic Diseases

Laboratory Testing in Coagulation

Quality Assessment in the Hematology Laboratory

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