HEMOSTASIS Flashcards
Which of the following lists the steps of the hemostatic response in the correct order?
a. Fibrinolysis → injury → secondary hemostasis → primary hemostasis
b. Injury → primary hemostasis → secondary hemostasis → fibrinolysis
c. Injury → secondary hemostasis → primary hemostasis → fibrinolysis
d. Injury → fibrinolysis → primary hemostasis → secondary hemostasis
b. Injury → primary hemostasis → secondary hemostasis → fibrinolysis
When damage occurs to the endothelium, primary hemostasis occurs first, resulting in the formation of the primary platelet plug. Secondary hemostasis occurs next, which results in the formation of a stable fibrin clot. The last action is fibrinolysis, which results in the breakdown of the clot.
Which of the following properties renders the vessel wall prothrombotic?
a. Negatively charged surface
b. Production of prostacyclin and nitric oxide
c. Release of tissue factor
d. Inactivation of thrombin
c. Release of tissue factor
Under normal circumstances, vessels are non-thrombotic. Factors that contribute to this include a negatively charged surface; the inhibition of platelet activation through prostacyclin, nitric oxide, and ADPase; and the inactivation of thrombin through heparin sulfate and thrombomodulin. Once damaged, tissue factor is one of the substances released that favors the formation of clots. Other prothrombotic substances include the secretion of platelet-activating factor and von Willebrand factor.
Which of the following is not true regarding platelets?
a. Platelets are not affected by aspirin
b. Platelets have a life span of 7 to 10 days
c. Platelets undergo shape change and develop pseudopods when activated
d. Von Willebrand factor serves as a bridge between platelets and collagen
a. Platelets are not affected by aspirin
Aspirin inhibits cyclooxygenase, which blocks thromboxane A2 (TXA2) synthesis, thereby making platelets nonfunctional for the life span of the platelets.
Which of the following factors binds to platelets via the glycoprotein IIb/IIIa receptor?
a. Von Willebrand factor
b. Factor II
c. Fibrinogen
d. Thrombin
c. Fibrinogen
Both fibrinogen and von Willebrand factor (vWF) bind to platelets. Fibrinogen binds to platelets via the GbIIb/IIIa receptor. vWF binds through the GpIb/IX receptor.
Which of the following is not an agonist of platelet aggregation?
a. Saline
b. ADP
c. Collagen
d. Epinephrine
a. Saline
Platelet agonists include collagen, adenosine diphosphate (ADP), thrombin, epinephrine, thromboxane A2 (TXA2), and arachidonic acid.
Which enzyme is blocked by the presence of aspirin?
a. Phospholipase A2
b. Cyclooxygenase
c. Protein kinase
d. ATPase
b. Cyclooxygenase
Aspirin inhibits cyclooxygenase, which blocks thromboxane A2 (TXA2) synthesis, thereby making platelets nonfunctional for their life span.
Secondary hemostasis occurs when a sufficient stimulus is present to cause the release of internal ADP, synthesis and release of thromboxane A2, and increased calcium release.
a. True
b. False
a. True
For secondary aggregation to occur, sufficient stimulus must be present. The stimulus occurs after internal adenosine diphosphate and calcium are released, along with the synthesis and release of thromboxane A2 (TXA2). Primary aggregation is reversible.
Which of the following factors is called prothrombin?
a. Fibrinogen
b. Factor II
c. Factor X
d. Factor XIII
b. Factor II
Factor II is also called prothrombin.
Which of the following factors usually results in no clinical bleeding when deficient?
a. Factor XII
b. Factor IX
c. Factor VIII
d. Factor VIi
a. Factor XII
A deficiency of factor XII, as well as prekallikrein and high-molecular-weight kininogen, does not usually manifest with clinical bleeding. Deficiencies of factors IX, VIII, and VII all generally present with clinical bleeding depending on the degree of deficiency.
The step necessary for the functionary factors II, VII, IX, and X is called the ______________ step.
a. Oxidation
b. Hydrolysis
c. Cleavage
d. γ-Carboxylation
d. γ-Carboxylation
Vitamin K is required for the γ-carboxylation step of the formation of factors II, VII, IX, and X and proteins C and S. In this step, an additional carboxyl group is added to the g-carbon of the glutamic acid residues on the factors. Without this step, the factor is formed, but is not functional because binding to a negatively charged phospholipid surface cannot occur.
Monitoring of the intrinsic pathway is accomplished by performing which of the following analytical tests?
a. PT
b. PTT
c. Thrombin time
d. Fibrinogen assay
b. PTT
The intrinsic pathway of hemostasis can be monitored through the partial thromboplastin time (PTT) assay. The prothrombin time (PT) assay can be used to monitor the extrinsic pathway. The thrombin time test assesses the formation of fibrin. The fibrinogen assay is used to measure fibrinogen levels.
Monitoring of the extrinsic pathway is accomplished by performing which of the following analytical tests?
a. PT
b. PTT
c. Thrombin time
d. Fibrinogen assay
a. PT
The prothrombin time (PT) assay can be used to monitor the extrinsic pathway. The intrinsic pathway of hemostasis can be monitored through the partial thromboplastin time (PTT) assay. The thrombin time test assesses the formation of fibrin. The fibrinogen assay is used to measure fibrinogen levels.
Which of the following cleaves the fibrinopeptides from fibrinogen?
a. Factor VIII
b. Thrombin
c. Tissue factor
d. Factor XIII
b. Thrombin
One of thrombin’s many actions is to cleave fibrinopeptides A and B from fibrinogen. This step results in the formation of a fibrin monomer, which can then continue to aggregate with other fibrin monomers. Factor VIII participates in the common pathway. Tissue factor is released by the endothelium during the initial stages leading to primary aggregation. Factor XIII is involved in the covalent cross-linking of D domains of fibrin to form a stable fibrin clot.
Activation of factor VII after the release of tissue factor initiates which of the following pathways?
a. Intrinsic pathway
b. Extrinsic pathway
c. Common pathway
d. Fibrinolytic pathway
b. Extrinsic pathway
Factor VII is involved in the extrinsic pathway of coagulation, along with tissue factor.
Which of the following is not true?
a. Factor VIII is a cofactor for factor IXa
b. Factor V is a cofactor for factor Xa
c. Protein K is a cofactor for protein C
d. High-molecular-weight kininogen is a cofactor for factor XIIa
c. Protein K is a cofactor for protein C
Protein S is a cofactor for protein C.
If a deficiency of this factor is present, the cross-linking of fibrin will not occur.
a. Factor II
b. Factor V
c. Factor XI
d. Factor XIII
d. Factor XIII
Factor XIII covalently cross-links the D domains of fibrin to form a urea-insoluble clot. Factors II, V, and XI are involved in other parts of the hemostasis pathway.
Factor VIII is protected from degradation when circulating in the plasma by its carrier protein __________.
a. Factor IX
b. Thrombin
c. Von Willebrand factor
d. Glycoprotein IIb/IIIa
c. Von Willebrand factor
Von Willebrand factor circulates as the vWF/VIII complex. If circulating alone, factor VIII will be quickly degraded.
Which of the following factors is associated with hemophilia B?
a. Factor VIII
b. Factor IX
c. Factor XI
d. Fibrinogen
b. Factor IX
A deficiency of factor IX is called hemophilia B. Hemophilia A is associated with a deficiency of factor VIII. Hemophilia C is associated with a deficiency of factor XI.
The activation of plasmin results in which of the following?
a. The formation of a fibrin clot
b. The formation of the bridge between platelets and the vessel wall
c. The start of the process to break down a fibrin clot
d. The point at which the intrinsic and extrinsic pathways feed into the common pathway
c. The start of the process to break down a fibrin clot
Fibrinolysis is the process of breaking down a fibrin clot. The activation of plasmin by plasminogen activators begins this process.
Which of the following proteins is degraded by plasmin?
a. Fibrin
b. Fibrinogen
c. A and B
d. None of the above
c. A and B
Plasmin is a serine protease with broad specificity against proteins that are susceptible to trypsin degradation. In terms of the hemostatic pathway, plasmin has an effect against fibrin, fibrinogen, and factors V and VIII.
Streptokinase differs from urokinase plasminogen activator (uPA) in that:
a. Streptokinase activates plasminogen to plasmin conversion, whereas uPA inhibits the conversion
b. uPA is effective only when given as a medication
c. Streptokinase is an exogenous activator, whereas uPA is a physiologic activator
d. No difference exists between streptokinase and uPA
c. Streptokinase is an exogenous activator, whereas uPA is a physiologic activator
There are physiologic and exogenous plasminogen activators. The exogenous plasminogen activators include streptokinase and staphylokinase. The physiologic plasminogen activators include tissue-type plasminogen activator and urokinase-type plasminogen activator.
Which of the following are fibrin degradation products?
a. Fragment X
b. Fragment Y
c. Fragment D
d. All of the above
d. All of the above
When plasmin cleaves fibrin, the breakdown products that are formed include fragment X, fragment Y, fragment D, and fragment E. Fragment X has a limited binding ability for thrombin. Fragments Y, D, and E all inhibit fibrin polymerization and inhibit platelet aggregation.
Which of the following describes the role of PAI-1 in hemostasis?
a. Plasminogen activator inhibitor–1 limits the activation of plasminogen
b. Plasminogen activator inhibitor–1 stimulates the activation of plasminogen
c. Plasminogen activator inhibitor–1 is involved in limiting clot formation in vessels
d. Plasminogen activator inhibitor–1 blocks platelet binding to the fibrin clot
a. Plasminogen activator inhibitor–1 limits the activation of plasminogen
Plasminogen activator inhibitor-1 has a significant role in limiting the activation of plasminogen.
Which of the following fibrinolytic inhibitors is useful when a2-antiplasmin activity has been exhausted?
a. PAI-1
b. Thrombin-activatable fibrinolysis inhibitor
c. a2-Macroglobulin
d. Plasminogen
c. a2-Macroglobulin
a2-Macroglobulin has wide specificity against many proteases. It generally is not used until a2-antiplasmin is consumed.