front 1 After a small vessel is ruptured, which immediate response reflects intrinsic smooth muscle contraction of the vessel wall itself? A. Endothelial budding | back 1 C. Myogenic spasm |
front 2 Damaged tissue can promote early postinjury vasoconstriction through locally released: A. Autacoid factors | back 2 A. Autacoid factors |
front 3 Which mechanism represents a contribution to immediate vasoconstriction after vascular injury? A. Collagen exposure | back 3 D. Nervous reflexes |
front 4 Ongoing platelet activity helps narrow a recently injured vessel by releasing: A. Fibrinopeptide B | back 4 B. Thromboxane A2 |
front 5 A superficial capillary nick stops bleeding before a stable fibrin mesh develops. The defect was most likely sealed initially by a: A. Platelet plug | back 5 A. Platelet plug |
front 6 Circulating thrombocytes arise from fragmentation of: A. Myeloblasts | back 6 C. Megakaryocytes |
front 7 Which platelet contractile protein is most directly involved in clot contraction? A. Talin | back 7 D. Thrombosthenin |
front 8 After endothelial denudation, platelets adhere most directly to exposed: A. Collagen and fibrin | back 8 B. Collagen and vWF |
front 9 Platelet surface glycoproteins participate in adhesion by binding: A. von Willebrand factor | back 9 A. von Willebrand factor |
front 10 Early during platelet aggregation, activated platelets release: A. Protein C and S | back 10 C. ADP and PAF |
front 11 Which group most directly amplifies recruitment of nearby platelets at an injury site? A. Factor XII, prekallikrein, HMWK | back 11 D. ADP, PAF, TXA2 |
front 12 A thrombocytopenic patient develops multiple pinpoint hemorrhages under the skin. These lesions are termed: A. Ecchymoses | back 12 B. Petechiae |
front 13 A formed clot that becomes organized during healing is most likely to undergo: A. Invasion by fibroblasts | back 13 A. Invasion by fibroblasts |
front 14 A small clot that disappears rather than becoming organized has most likely undergone: A. Ossification | back 14 D. Dissolution |
front 15 The first general step in coagulation is: A. Fibrin cross-linking | back 15 B. Prothrombin activator formation |
front 16 The second general step of coagulation is best described as: A. Factor XIII activation | back 16 C. Prothrombin to thrombin |
front 17 The final general step in clot formation is: A. Fibrinogen to fibrin | back 17 A. Fibrinogen to fibrin |
front 18 Factor Xa most directly converts prothrombin to thrombin in the presence of sufficient: A. ADP | back 18 D. Ca2+ |
front 19 The rate-limiting event in blood coagulation is the formation of: A. Thrombin | back 19 C. Prothrombin activator |
front 20 Prothrombin is synthesized primarily in the: A. Spleen | back 20 B. Liver |
front 21 A patient with impaired vitamin-dependent hepatic clotting function would have defective normal activation of prothrombin because the liver requires vitamin: A. K | back 21 A. K |
front 22 Fibrinogen is synthesized primarily in the: A. Spleen | back 22 A. Spleen |
front 23 In coagulation, thrombin functions primarily as a: A. Carrier protein | back 23 B. Protease |
front 24 Once fibrin strands are formed, the reticulum is strengthened by: A. Thromboxane A2 | back 24 C. Fibrin stabilizing factor |
front 25 A laboratory specimen forms a clot but fails to retract appropriately. This finding most strongly suggests decreased: A. Circulating platelets | back 25 A. Circulating platelets |
front 26 In this material, fibrin stabilizing factor is released by: A. Hepatocytes | back 26 D. Platelets |
front 27 Thrombin exerts what effect on its own generation? A. No meaningful feedback | back 27 B. Positive feedback |
front 28 A patient with extensive soft-tissue trauma develops rapid coagulation through the pathway initiated outside the bloodstream. Which pathway is most directly involved? A. Common pathway | back 28 C. Extrinsic pathway |
front 29 In contrast to the extrinsic pathway, the intrinsic pathway is best characterized by which initiating feature? A. Begins in the blood | back 29 A. Begins in the blood |
front 30 A crush injury to skeletal muscle rapidly activates coagulation because trauma to the vascular wall and surrounding tissues preferentially triggers the: A. Protein C pathway | back 30 B. Extrinsic pathway |
front 31 The first major event in the extrinsic pathway is release of: A. Prekallikrein | back 31 C. Tissue factor |
front 32 Traumatized tissue releases which substance to initiate the extrinsic cascade? A. Thromboplastin | back 32 A. Thromboplastin |
front 33 In the extrinsic pathway, tissue factor complexes with which factor before activation of factor X? A. Factor V | back 33 B. Factor VII |
front 34 In tissue injury, factor X is most directly converted to Xa by the combination of: A. VIIIa and IXa | back 34 D. VII and tissue factor |
front 35 Which event occurs immediately after factor X activation in the extrinsic pathway? A. Fibrin degradation | back 35 C. Xa forms prothrombin activator |
front 36 In the extrinsic pathway, prothrombin is split to thrombin in the presence of: A. HMW kininogen | back 36 C. Calcium |
front 37 Which factor accelerates protease activity in the extrinsic pathway and promotes more clotting by positive feedback? A. Factor II | back 37 B. Factor V |
front 38 A coagulation defect selectively impairing the accelerating factor of the extrinsic pathway would most directly involve: A. Factor V | back 38 A. Factor V |
front 39 A researcher compares clotting pathways and notes one is triggered by trauma to blood itself or exposure of blood to collagen. This describes the: A. Extrinsic pathway | back 39 C. Intrinsic pathway |
front 40 Exposure of blood to subendothelial collagen most directly instigates the: A. Extrinsic pathway | back 40 B. Intrinsic pathway |
front 41 The earliest intrinsic-pathway event after blood trauma is activation of factor XII along with release of: A. Protein C | back 41 B. Platelet phospholipids |
front 42 When blood trauma occurs, platelet phospholipids release: A. PF3 | back 42 A. PF3 |
front 43 In the intrinsic pathway, factor XIIa converts factor XI to XIa only in the presence of: A. Tissue factor | back 43 C. HMW kininogen |
front 44 Which substance accelerates the conversion of factor XI to XIa during intrinsic coagulation? A. Citrate | back 44 B. Prekallikrein |
front 45 In the intrinsic pathway, factor XIa most directly converts: A. VIII to VIIIa | back 45 C. IX to IXa |
front 46 Activation of factor X through the intrinsic pathway requires IXa acting together with VIIIa, platelet phospholipids, and: A. Factor III | back 46 A. Factor III |
front 47 Which combination is required for intrinsic activation of factor X? A. VIIa, tissue factor, calcium | back 47 C. IXa, VIIIa, III, phospholipids |
front 48 After factor X becomes Xa in the intrinsic pathway, Xa forms prothrombin activator with assistance from: A. Factor V | back 48 A. Factor V |
front 49 Following formation of prothrombin activator in the intrinsic pathway, the next step is: A. XI to XIa | back 49 B. Prothrombin to thrombin |
front 50 The final step listed in the intrinsic pathway is conversion of: A. Thrombin to prothrombin | back 50 C. Fibrinogen to fibrin |
front 51 Compared with the extrinsic pathway, the intrinsic pathway generally occurs: A. Faster | back 51 B. Slower |
front 52 Contact of factor XII and platelets with collagen most directly initiates the: A. Extrinsic pathway | back 52 B. Intrinsic pathway |
front 53 A phlebotomy specimen is prevented from clotting by chemically reducing ionized calcium. Which additive could achieve this? A. Heparin only | back 53 C. Citrate |
front 54 Which additive also prevents clotting in removed blood by reducing available calcium? A. Oxalate | back 54 A. Oxalate |
front 55 Which endothelial property normally helps prevent contact activation of the intrinsic clotting system? A. Surface smoothness | back 55 A. Surface smoothness |
front 56 The endothelial glycocalyx helps prevent coagulation primarily by: A. Activating factor XII | back 56 B. Repelling clotting factors |
front 57 Which endothelial membrane-bound molecule contributes to prevention of clotting in normal vessels? A. Thrombomodulin | back 57 A. Thrombomodulin |
front 58 Thrombomodulin bound to thrombin most directly activates: A. Protein C | back 58 A. Protein C |
front 59 Activated protein C exerts anticoagulant effects by inactivating which factors? A. II and VII | back 59 B. V and VIII |
front 60 Two prominent endothelial vasodilators that inhibit platelet aggregation are: A. NO and PGI2 | back 60 A. NO and PGI2 |
front 61 Which prostanoid released by endothelium inhibits platelet aggregation? A. TXA2 | back 61 B. PGI2 |
front 62 An important circulating anticoagulant that removes thrombin from blood is: A. Protein C | back 62 C. Antithrombin III |
front 63 Besides antithrombin III, which structure in a developing clot can help remove thrombin? A. Fibrin fibers | back 63 A. Fibrin fibers |
front 64 Heparin exerts its major anticoagulant effect in this material by binding to antithrombin III and increasing removal of: A. Fibrinogen | back 64 B. Thrombin |
front 65 Heparin bound to antithrombin III inactivates which activated clotting-factor range? A. IIa–V | back 65 C. IXa–XIIa |
front 66 A hospitalized patient receives heparin. Its anticoagulant action is enhanced because heparin is working with: A. Tissue factor | back 66 B. Antithrombin III |
front 67 Heparin is released primarily by: A. Neutrophils | back 67 C. Mast cells |
front 68 Which enzyme digests fibrin and also degrades fibrinogen, factor V, factor VIII, prothrombin, and factor XII? A. Thrombin | back 68 B. Plasmin |
front 69 Conversion of plasminogen to plasmin is catalyzed by: A. PF3 | back 69 C. t-PA |
front 70 A patient receives thrombolytic therapy for an acute clot. The drug most directly mimics the action of: A. Tissue plasminogen activator | back 70 A. Tissue plasminogen activator |
front 71 One of the classic major causes of excessive bleeding? A. Hemophilia | back 71 A. Hemophilia |
front 72 A malnourished patient with prolonged coagulation studies has excessive bleeding due to deficiency of which factor-related nutrient? A. Vitamin K | back 72 A. Vitamin K |
front 73 A patient with diffuse petechiae and a markedly decreased platelet count has excessive bleeding due to: A. Hemophilia | back 73 D. Thrombocytopenia |
front 74 Vitamin K serves as a cofactor for which hepatic enzyme type? A. Protease | back 74 B. Carboxylase |
front 75 Vitamin K–dependent carboxylation directly modifies which clotting factor? A. Factor VIII | back 75 B. Factor II |
front 76 Which clotting factor also requires vitamin K–dependent carboxylation in the liver? A. Factor VIII | back 76 D. Factor VII |
front 77 A defect in vitamin K–dependent carboxylation would impair activation of which additional factor? A. Factor IX | back 77 A. Factor IX |
front 78 Vitamin K deficiency would also reduce proper hepatic modification of: A. Factor XI | back 78 C. Factor X |
front 79 Which anticoagulant protein is included among the vitamin K–dependent carboxylated proteins? A. Protein C | back 79 A. Protein C |
front 80 Vitamin K is recycled back to its active form by: A. Cyclooxygenase | back 80 D. VKORC1 |
front 81 Hemophilia occurs almost exclusively in: A. Males | back 81 A. Males |
front 82 Most cases of hemophilia are caused by deficiency of: A. Factor IX | back 82 D. Factor VIII |
front 83 A patient with the less common classic hemophilia variant has deficiency of: A. Factor VIII | back 83 B. Factor IX |
front 84 Deficiency of factor IX is specifically termed: A. von Willebrand disease | back 84 D. Hemophilia B |
front 85 In hemophilia A, the primarily affected coagulation pathway is the: A. Extrinsic pathway | back 85 C. Intrinsic pathway |
front 86 Loss of the larger component of factor VIII produces: A. Hemophilia B | back 86 D. von Willebrand disease |
front 87 A patient develops thrombocytopenia after an infiltrative infectious process involving the marrow. Which mechanism best explains the low platelet count? A. Bone marrow infection | back 87 A. Bone marrow infection |
front 88 A patient with autoimmune platelet destruction has thrombocytopenia due to: A. Portal hypertension | back 88 D. Antibody-mediated destruction |
front 89 A cirrhotic patient with portal hypertension has thrombocytopenia mainly because of: A. Marrow suppression | back 89 B. Splenic sequestration |
front 90 Widespread microvascular clotting may lower platelet count through: A. Decreased thrombopoiesis | back 90 C. Platelet consumption in thrombi |
front 91 A massively transfused trauma patient develops low platelets primarily because of: A. Dilution from transfusion | back 91 A. Dilution from transfusion |
front 92 In selected patients with thrombocytopenia, which intervention may be beneficial? A. Hepatectomy | back 92 B. Splenectomy |
front 93 An abnormal clot forming within an intact blood vessel is called a: A. Embolus | back 93 D. Thrombus |
front 94 A detached intravascular clot traveling in the circulation is a: A. Embolus | back 94 A. Embolus |
front 95 A lower-extremity clot that dislodges and obstructs the pulmonary arteries causes: A. Cerebral embolism | back 95 B. Pulmonary embolism |
front 96 Septicemia may trigger simultaneous diffuse coagulation and consumption known as: A. TTP | back 96 D. DIC |
front 97 Warfarin therapy lowers levels of which vitamin K–dependent factor? A. Factor IX | back 97 A. Factor IX |
front 98 Coumarin therapy also decreases which factor most associated with the extrinsic pathway? A. Factor VIII | back 98 D. Factor VII |
front 99 Warfarin lowers which precursor listed in this material? A. Active prothrombin | back 99 A. Active prothrombin |
front 100 Which additional factor falls with warfarin use? A. Factor V | back 100 B. Factor X |
front 101 Warfarin most directly inhibits which enzyme? A. Thrombin | back 101 C. VKORC1 |
front 102 Exposure of blood to silicon inactivates platelets and: A. Factor IX | back 102 D. Factor XII |
front 103 Removal of ionized calcium from blood will produce: A. More coagulation | back 103 C. Less coagulation |
front 104 Bleeding time most directly evaluates: A. Platelet levels | back 104 A. Platelet levels |
front 105 Prothrombin time is primarily used to evaluate the: A. Intrinsic pathway | back 105 D. Extrinsic pathway |
front 106 The normal INR range given in this material is: A. 2.0 to 3.0 | back 106 B. 0.9 to 1.3 |
front 107 A markedly elevated INR most strongly indicates: A. Risk of bleeding | back 107 A. Risk of bleeding |
front 108 A low INR most strongly suggests: A. Factor VIII deficiency | back 108 D. High chance of clot |
front 109 A patient appropriately anticoagulated with warfarin should generally have an INR of: A. 2.0 to 3.0 | back 109 A. 2.0 to 3.0 |
front 110 Classic hemophilia differs from von Willebrand disease in this material because classic hemophilia reflects loss of the: A. Larger VIII component | back 110 C. Smaller VIII component |