21.-2.4 Hemostasis and Thrombosis

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  • 1. Which of the following initiates in vivo coagulation by activation of factor VII?
    A. Protein C
    B. Tissue factor
    C. Plasmin activator
    D. Thrombomodulin
    B
  • 2. Which of the following clotting factors plays a role in clot formation in vitro, but not in vivo? in vitro clot formation and not in vivo coagulation?
    A. VIIa
    B. IIa
    C. XIIa
    D. Xa
    C
  • 3. The anticoagulant of choice for most routine coagulation studies is: A. Sodium oxalate
    B. Sodium citrate
    C. Heparin
    D. Ethylenediaminetetraacetic acid (EDTA)
    3. B The anticoagulant of choice for most coagulation procedures is sodium citrate (3.2%). Because factors V and VIII are more labile in sodium oxalate, heparin neutralizes thrombin, and EDTA inhibits thrombin's action on fibrinogen, these anticoagulants are not used for routine coagulation studies
  • 4. Which ratio of anticoagulant-to-blood is correct for coagulation procedures?
    A. 1:4
    B. 1:5
    C. 1:9
    D. 1:10
    4. C The optimum ratio of anticoagulant to blood is one part anticoagulant to nine parts of blood. The anticoagulant supplied in this amount is sufficient to bind all the available calcium, thereby preventing clotting.
  • 5. Which results would be expected for the prothrombin time (PT) and activated partial thromboplastin time (APTT) in a patient with polycythemia?
    A. Both prolonged
    B. Both shortened
    C. Normal PT, prolonged APTT
    D. Both normal
    5. A The volume of blood in a polycythemic patient contains so little plasma that excess anticoagulant remains and is available to bind to reagent calcium, thereby resulting in prolongation of the PT and APTT. For more accurate results, the plasma:anticoagulant ratio can be modified by decreasing the amount of anticoagulant in the collection tube using the following formula: (0.00185)(V)(100-H) = C, where V = blood volume in mL; H = patient's Hct; and C = volume (mL) of anticoagulant. A new sample should be drawn to rerun the PT and APTT.
  • 6. What reagents are used in the PT test?
    A. Thromboplastin and sodium chloride
    B. Thromboplastin and potassium chloride
    C. Thromboplastin and calcium
    D. Actin and calcium chloride
    6. C Thromboplastin and calcium (combined into a single reagent) replace the tissue thromboplastin and calcium necessary in vivo to activate factor VII to factor VIIa. This ultimately generates thrombin from prothrombin via the coagulation cascade.
  • 7. Which test would be abnormal in a patient with factor X deficiency? A. PT only
    B. APTT only
    C. PT and APTT
    D. Thrombin time
    7. C Factor X is involved in the common pathway of the coagulation cascade; therefore, its deficiency prolongs both the PT and APTT. Activated factor X along with factor V in the presence of calcium and platelet factor III (PF3) converts prothrombin (factor II) to the active enzyme thrombin (factor IIa).
  • 8. Which clotting factor is not measured by PT and APTT tests?
    A. Factor VIII
    B. Factor IX
    C. Factor V
    D. Factor XIII
    8. D Factor XIII is not measured by the PT or APTT. Factor XIII (fibrin stabilizing factor) is a transamidase. It creates covalent bonds between fibrin monomers formed during the coagulation process to produce a stable fibrin clot. In the absence of factor XIII, the hydrogen bonded fibrin polymers are soluble in 5M urea or in 1% monochloroacetic acid.
  • 9. A modification of which procedure can be used to measure fibrinogen?
    A. PT
    B. APTT
    C. Thrombin time
    D. Fibrin degradation products
    9. C Fibrinogen can be quantitatively measured by a modification of the thrombin time by diluting the plasma, because the thrombin clotting time of diluted plasma is inversely proportional to the concentration of fibrinogen (principle of Clauss method).
  • 10. Which of the following characterizes vitamin K?
    A. It is required for biological activity of fibrinolysis
    B. Its activity is enhanced by heparin therapy
    C. It is required for carboxylation of glutamate residues of some coagulation factors
    D. It is made by the endothelial cells
    10. C Vitamin K is necessary for activation of vitamin K- dependent clotting factors (II, VII, IX, and X). This activation is accomplished by carboxylation of glutamic acid residues of the inactive clotting factors. The activity of vitamin K is not enhanced by heparin therapy. Vitamin K is present in a variety of foods and is also the only vitamin made by the organisms living in the intestine
  • 11. Which statement about the fibrinogen/fibrin degradation product test is correct?
    A. It detects early degradation products (X and Y)
    B. It is decreased in disseminated intravascular coagulation (DIC)
    C. It evaluates the coagulation system
    D. It detects late degradation products (D and E)
    11. D The fibrin degradation product (FDP) test detects the late degradation products (fragments D and E) and not the early ones (fragments X and Y).
  • 12. Which of the following clotting factors are measured by the APTT test?
    A. II, VII, IX, X
    B. VII, X, V, II, I
    C. XII, XI, IX, VIII, X, V, II, I
    D. XII, VII, X, V, II, I
    12. C The APTT test evaluates the clotting factors in the intrinsic pathway (XII, XI, IX, and VIII) as well as the common pathway (X, V, II, and I).
  • 13. Which coagulation test(s) would be abnormal in a vitamin K-deficient patient?
    A. PT only
    B. PT and APTT
    C. Fibrinogen level
    D. Thrombin time

    13. B Patients with vitamin K deficiency exhibit decreased production of functional prothrombin proteins (factors II, VII, IX, and X). Decreased levels of these factors prolong both the PT and APTT.
  • 14. Which of the following is correct regarding the international normalized ratio (INR)?
    A. It uses the International Sensitivity Ratio (ISR)
    B. It standardizes PT results
    C. It standardizes APTT results
    D. It is used to monitor heparin therapy
    14. B INR is used to standardize PT results to adjust for the difference in thromboplastin reagents made by different manufacturers and used by various institutions. The INR calculation uses the International Sensitivity Index (ISI) value, and is used to monitor an oral anticoagulant such as warfarin. INR is not used to standardize APTT testing.
  • 15. Which of the following is referred to as an endogenous activator of plasminogen?
    A. Streptokinase
    B. Transamidase
    C. Tissue plasminogen activator
    D. Tissue plasminogen activator inhibitor
    15. C Tissue plasminogen activator (tPA) is an endogenous (produced in the body) activator of plasminogen. It is released from the endothelial cells by the action of protein C. It converts plasminogen to plasmin. Streptokinase is an exogenous (not made in the body) activator of plasminogen.
  • 16. Which protein is the primary inhibitor of the fibrinolytic system?
    A. Protein C
    B. Protein S
    C. α2-Antiplasmin
    D. α2-Macroglobulin
    16. C α2-Antiplasmin is the main inhibitor of plasmin. It inhibits plasmin by forming a 1:1 stoichiometric complex with any free plasmin in the plasma and, therefore, prevents the binding of plasmin to fibrin and fibrinogen.
  • 17. Which of the following statements is correct regarding the D-dimer test?
    A. Levels are decreased in DIC
    B. Test detects polypeptides A and B
    C. Test detects fragments D and E
    D. Test has a negative predictive value
    17. D The D-dimer assay evaluates fibrin degradation. It is a nonspecific screening test that is increased in many conditions in which fibrinolysis is increased, such as DIC and fibrinolytic therapy. The D-dimer test is widely used to rule out thrombosis and thrombotic activities. The negative predictive value of a test is the probability that a person with a negative result is free of the disease the test is meant to detect. Therefore, a negative D-dimer test rules out thrombosis and hence further laboratory investigations are not required
  • 18. A protein that plays a role in both coagulation and platelet aggregation is:
    A. Factor I
    B. Factor VIII
    C. Factor IX
    D. Factor XI
    18. A Factor I (fibrinogen) is necessary for platelet aggregation along with the glycoprotein IIb/IIIa complex. Factor I is also a substrate in the common pathway of coagulation. Thrombin acts on fibrinogen to form fibrin clots
  • 19. A standard 4.5-mL blue-top tube filled with 3.0 mL of blood was submitted to the laboratory for PT and APTT tests. The sample is from a patient undergoing surgery the following morning for a tonsillectomy. Which of the following is the necessary course of action by the technologist?
    A. Run both tests in duplicate and report the average result
    B. Reject the sample and request a new sample
    C. Report the PT result
    D. Report the APTT result
    19. B A 4.5-mL blue-top tube contains 4.5 mL blood + 0.5 mL sodium citrate. The tube should be 90% full. A tube with 3.0 mL blood should be rejected as quantity not sufficient (QNS). QNS samples alter the necessary blood to an anticoagulant ratio of 9:1. The excess anticoagulant in a QNS sample binds to the reagent calcium, thereby resulting in prolongation of the PT and APTT.
  • 20. Which statement is correct regarding sample storage for the prothrombin time test?
    A. Stable for 24 hours if the sample is capped
    B. Stable for 24 hours if the sample is refrigerated at 4°C
    C. Stable for 4 hours if the sample is stored at 4°C
    D. Should be run within 8 hours

    20. A According to Clinical Laboratory Standards Institute (CLSI, formerly NCCLS) guidelines, plasma samples for PT testing are stable for 24 hours at room temperature if capped. Refrigerating the sample causes cold activation of factor VII and, therefore, shortened PT results. The APTT samples are stable for 4 hours if stored at 4°C.
  • 21. In primary fibrinolysis, the fibrinolytic activity results in response to:
    A. Increased fibrin formation
    B. Spontaneous activation of fibrinolysis
    C. Increased fibrin monomers
    D. DIC
    21. B Primary fibrinolysis is a rare pathological condition in which a spontaneous systemic fibrinolysis occurs. Plasmin is formed in the absence of coagulation activation and clot formation. Primary fibrinolysis is associated with increased production of plasminogen and plasmin, decreased plasmin removal from the circulation, and spontaneous bleeding.
  • 22. Plasminogen deficiency is associated with:
    A. Bleeding
    B. Thrombosis
    C. Increased fibrinolysis
    D. Increased coagulation

    22. B Plasminogen deficiency is associated with thrombosis. Plasminogen is an important component of the fibrinolytic system. Plasminogen is activated to plasmin, which is necessary for degradation of fibrin clots to prevent thrombosis. When plasminogen is deficient, plasmin is not formed, causing a defect in the clot lysing processes
  • 23. Which of the following clotting factors are activated by thrombin that is generated by tissue pathway (TF-VIIa)?
    A. XII, XI
    B. XII, I
    C. I, II
    D. V, VIII
    23. D Factors V and VIII are activated by the thrombin that is generated by the action of TF-VIIa on factor X to form factor Xa. Factor Xa forms a complex with factor Va on the platelet surfaces. FXa -Va complex in the presence of phospholipid and Ca+2 transform more prothrombin to thrombin.
  • 24. What substrate is used in a chromogenic factor assay?
    A. p-nitroanaline
    B. Chloropheonol red
    C. Prussian blue
    D. Ferricyanide
    24. A The chromogenic, or amidolytic, assays use a color-producing substance known as a chromophore. The chromophore used for the coagulation laboratory is p-nitroaniline (pNa). The pNa is bound to a synthetic oligopeptide substrate. The protease cleaves the chromogenic substrate at the site binding the oligopeptide to the pNA, which results in release of pNA. Free pNA has a yellow color; the color intensity of the solution is proportional to the protease activity and is measured by a photodetector at 405 nm.
  • 25. Which of the following antibodies is used in the D-dimer assay?
    A. Polyclonal directed against X and Y fragments
    B. Polyclonal directed against D-dimer
    C. Monoclonal against D and E fragments
    D. Monoclonal against D-dimer

    25. D The D-dimer is the fibrin degradation product generated by the action of plasmin on cross-linked fibrin formed by XIIIa. The patient plasma is mixed with latex particles coated with monoclonal antibodies against D-domains. The test can be automated or performed manually on a glass slide, looking macroscopically for agglutination. ELISA methods are also available. Normal D-dimer in plasma is less than 2 ng/mL. Increased levels of D-dimer are associated with DIC, thrombolytic therapy, venous thrombosis, and thromboembolic disorders. The D-dimer assay has a 90%-95% negative predictive value, and has been used to rule out thrombosis and thromboembolic disorders.
  • 2.2 Platelet and Vascular Disorders
    2.2 Platelet and Vascular Disorders
  • 1. Thrombotic thrombocytopenic purpura (TTP) is characterized by:
    A. Prolonged PT
    B. Increased platelet aggregation
    C. Thrombocytosis
    D. Prolonged APTT
    1. B Thrombotic thrombocytopenic purpura (TTP) is a quantitative platelet disorder associated with increased intravascular platelet activation and aggregation resulting in thrombocytopenia. The PT and APTT results are normal in TTP.
  • 2. Thrombocytopenia may be associated with:
    A. Postsplenectomy
    B. Hypersplenism
    C. Acute blood loss
    D. Increased proliferation of pluripotential stem cells

    2. B Hypersplenism is associated with thrombocytopenia. In this condition, up to 90% of platelets can be sequestered in the spleen, causing decreases in circulatory platelets. Postsplenectomy, acute blood loss, and increased proliferation of pluripotential stem cells are associated with thrombocytosis.
  • 3. Aspirin prevents platelet aggregation by inhibiting the action of which enzyme?
    A. Phospholipase
    B. Cyclo-oxygenase
    C. Thromboxane A2 synthetase
    D. Prostacyclin synthetase

    3. B Aspirin prevents platelet aggregation by inhibiting the activity of the enzyme cyclo-oxygenase. This inhibition prevents the formation of thromboxane A2 (TXA2), which serves as a potent platelet aggregator.
  • 4. Normal platelet adhesion depends upon:
    A. Fibrinogen
    B. Glycoprotein Ib
    C. Glycoprotein IIb, IIIa complex
    D. Calcium
    4. B Glycoprotein Ib is a platelet receptor for VWF. Glycoprotein Ib and VWF are both necessary for a normal platelet adhesion. Other proteins that play a role in platelet adhesion are glycoproteins V and IX.
  • 5. Which of the following test results is normal in a patient with classic von Willebrand's disease?
    A. Bleeding time
    B. Activated partial thromboplastin time
    C. Platelet count
    D. Factor VIII:C and von Willebrand's factor (VWF) levels
    5. C Von Willebrand's disease is an inherited, qualitative platelet disorder resulting in increased bleeding, prolonged APTT, and decreased factor VIII:C and VWF levels. The platelet count and morphology are generally normal in von Willebrand's disease, but aggregation in the platelet function assay is abnormal.
  • 6. Bernard-Soulier syndrome is associated with:
    A. Decreased bleeding time
    B. Decreased factor VIII assay
    C. Thrombocytopenia and giant platelets
    D. Abnormal platelet aggregation to ADP
    6. C Bernard-Soulier syndrome is associated with thrombocytopenia and giant platelets. It is a qualitative platelet disorder caused by the deficiency of glycoprotein Ib. In Bernard-Soulier syndrome, platelet aggregation to ADP is normal. Aggregation in the platelet function assay is abnormal. Factor VIII assay is not indicated for this diagnosis.
  • 7. When performing platelet aggregation studies, which set of platelet aggregation results would most likely be associated with Bernard-Soulier syndrome?
    A. Normal platelet aggregation to collagen, ADP, and ristocetin
    B. Normal platelet aggregation to collagen, ADP, and epinephrine; decreased aggregation to ristocetin
    C. Normal platelet aggregation to epinephrine and ristocetin; decreased aggregation to collagen and ADP
    D. Normal platelet aggregation to epinephrine, ristocetin, and collagen; decreased aggregation to ADP

    7. B Bernard-Soulier syndrome is a disorder of platelet adhesion caused by deficiency of glycoprotein Ib. Platelet aggregation is normal in response to collagen, ADP, and epinephrine but abnormal in response to ristocetin
  • 8. Which set of platelet responses would be most likely associated with Glanzmann's thrombasthenia?
    A. Normal platelet aggregation to ADP and ristocetin; decreased aggregation to collagen
    B. Normal platelet aggregation to collagen; decreased aggregation to ADP and ristocetin
    C. Normal platelet aggregation to ristocetin; decreased aggregation to collagen, ADP, and epinephrine
    D. Normal platelet aggregation to ADP; decreased aggregation to collagen and ristocetin
    8. C Glanzmann's thrombasthenia is a disorder of platelet aggregation. Platelet aggregation is normal in response to ristocetin, but abnormal in response to collagen, ADP, and epinephrine.
  • 9. Which of the following is a characteristic of acute immune thrombocytopenic purpura?
    A. Spontaneous remission within a few weeks
    B. Predominantly seen in adults
    C. Nonimmune platelet destruction
    D. Insidious onset
    9. A Acute immune thrombocytopenic purpura is an immune-mediated disorder found predominantly in children. It is commonly associated with infection (primarily viral). It is characterized by abrupt onset, and spontaneous remission usually occurs within several weeks.
  • 10. TTP differs from DIC in that:
    A. APTT is normal in TTP but prolonged in DIC
    B. Schistocytes are not present in TTP but are present in DIC
    C. Platelet count is decreased in TTP but normal in DIC
    D. PT is prolonged in TTP but decreased in DIC

    10. A Thrombotic thrombocytopenic purpura is a platelet disorder in which platelet aggregation increases, resulting in thrombocytopenia. Schistocytes are present in TTP as a result of microangiopathic hemolytic anemia; however, the PT and APTT are both normal. In DIC, the PT and APTT are both prolonged, the platelet count is decreased, and schistocytes are seen in the peripheral smear.
  • 11. Several hours after birth, a baby boy develops petechiae and purpura and a hemorrhagic diathesis. The platelet count is 18 × 109/L. What is the most likely explanation for the low platelet count?
    A. Drug-induced thrombocytopenia
    B. Secondary thrombocytopenia
    C. Neonatal alloimmune thrombocytopenia
    D. Neonatal DIC
    11. C Neonatal alloimmune thrombocytopenia is similar to the hemolytic disease of the fetus and newborn. It results from immunization of the mother by fetal platelet antigens. The offending antibodies are commonly anti HPA-1a alloantibodies that are directed against glycoproteins IIb/IIIa, Ib/IX, Ia/IIb, and CD 109. The maternal antibodies cross the placenta, resulting in thrombocytopenia in the fetus.
  • 12. Which of the following is associated with post-transfusion purpura (PTP)?
    A. Nonimmune thrombocytopenia/alloantibodies
    B. Immune-mediated thrombocytopenia/ alloantibodies
    C. Immune-mediated thrombocytopenia/ autoantibodies
    D. Nonimmune-mediated thrombocytopenia/ autoantibodies
    12. B Post-transfusion purpura is a rare form of alloimmune thrombocytopenia characterized by severe thrombocytopenia following transfusion of blood or blood products. PTP is caused by antibody-related platelet destruction in previously immunized patients. In the majority of cases, the alloantibody produced is against platelet antigen A1 (PlA1), also referred to as HPA-1a
  • 13. Hemolytic uremic syndrome (HUS) is associated with:
    A. Fever, thrombocytosis, anemia, and renal failure
    B. Fever, granulocytosis, and thrombocytosis
    C. Escherichia coli 0157:H7
    D. Leukocytosis and thrombocytosis
    13. C HUS is caused by E. coli 0157:H7. It is associated with ingestion of E. coli-contaminated foods and is commonly seen in children. The clinical manifestations in HUS are fever, diarrhea, thrombocytopenia, microangiopathic hemolytic anemia, and renal failure.
  • 14. Storage pool deficiencies are defects of:
    A. Platelet adhesion
    B. Platelet aggregation
    C. Platelet granules
    D. Platelet production

    14. C Storage pool deficiencies are defects of platelet granules. Most commonly, a decrease in platelet-dense granules is present with decreased release of ADP, ATP, calcium, and serotonin from platelet-dense granules.