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26 Cards in this Set

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Coagulation Factor I. What is its Name and Function/Active Form?
I, aka Fibrinogen, has the function/active form of: Fibrin
Coagulation Factor II. What is its Name and Function/Active Form?
II, aka Prothrombin, has the function/active form of Serine protease
Coagulation Factor III. What is its Name and Function/Active Form?
III, aka Tissue factor, has the function/active form of Receptor and cofactor
Coagulation Factor IV. What is its Name and Function/Active Form?
IV, aka Ca2+, has the function/active form of Cofactor
Coagulation Factor V. What is its Name and Function/Active Form?
V, aka Proaccelerin, labile factor, has the function/active form of Cofactor
Coagulation Factor VII. What is its Name and Function/Active Form?
VII, aka Proconvertin, has the function/active form of Serine protease
Coagulation Factor VIII. What is its Name and Function/Active Form?
VIII, aka Antihemophilia factor A, has the function/active form of Cofactor
Coagulation Factor IX. What is its Name and Function/Active Form?
IX, aka Antihemophilia factor B, Christmas factor, has the function/active form of Serine protease
Coagulation Factor X. What is its Name and Function/Active Form?
X, aka Stuart-Prower factor, has the function/active form of Serine protease
Coagulation Factor XI. What is its Name and Function/Active Form?
XI, aka Plasma thromboplastin antecedent, has the function/active form of Serine protease
Coagulation Factor XIII. What is its Name and Function/Active Form?
XIII, aka Fibrin-stabilizing factor, has the function/active form of Ca2+-dependent transglutaminase
What is the function of Thrombomodulin?
Endothelial cell receptor, binds thrombin
What is the function of Protein C?
Activated by thrombomodulin-bound thrombin; is a serine protease
What is the function of Protein S?
cofactor; binds activated protein C
The clotting cascade consists of a series of protease activation steps leading to the activation of _____, which converts fibrinogen to fibrin.
thrombin
Thrombin also activates _____, which cross-links the fibrin and leads to “hard clot” formation.
transglutaminase,
Proteins S and C regulate the clotting cascade, and are activated by _____.
thrombin.
______ are serine protease inhibitors; for example, one of these is known as antithrombin III (ATIII) and aids in regulating blood coagulation by modulating thrombin activity.
Serpins
Heparin enhances the interaction of thrombin with ____.
ATIII, which modulates thrombin activity.
What is the only protease that can dissolve fibrin clots.?
Plasmin, the active product of plasminogen
Hemophilia A is due to a lack of factor ____, an essential factor required for thrombin activation
VIII
1. The edema observed in patients with non–calorie protein malnutrition is due to which of the following?(A) Loss of muscle mass(B) Ingestion of excess carbohydrates(C) Increased fluid uptake(D) Reduced protein synthesis in the liver(E) Increased production of ketone bodies
1. The answer is D. Under conditions of reduced protein ingestion, essential amino acids are scarce and the liver reduces protein synthesis, including circulating plasma proteins. The reduction of protein in the plasma results in a lower osmotic pressure, so excess fluid in the extravascular spaces cannot return to the blood, and remains outside of the circulation, collecting in tissues.
2. A recent surgery patient receiving warfarin therapy was found to be bleeding internally. The clotting process is impaired in this patient primarily because of which of the following?(A) Inability of the liver to synthesize clotting factors(B) Specific inhibition of Factor XIII activation(C) Inability to form clotting factor complexes on membranes(D) Reduction of plasma calcium levels(E) Enhancement of protein C activity
2. The answer is C. Warfarin inhibits the reduction of vitamin K epoxide, so active vitamin K levels decrease. The reduction in active vitamin K levels reduces the γ-carboxylation of clotting factors. In the absence of γ-carboxylation the clotting factors cannot bind to calcium to form membrane-associated complexes with other clotting factors. Warfarin has no effect on the liver's ability to synthesize the clotting factor (the synthesized factor is not modified), nor does warfarin specifically inhibit the activation of factor XIII. The inhibition is more global than just attacking one step in the coagulation cascade. Plasma calcium levels are not altered by warfarin, and protein C activity is actually decreased in the presence of warfarin, because protein C is one of the proteins that is γ-carboxylated in a vitamin K–dependent reaction.
3. An inactivating mutation in which of the following proenzymes would be expected to lead to thrombosis, uncontrolled blood clotting?(A) Factor XIII(B) Prothrombin(C) Protein C(D) Factor VIII(E) Tissue factor
3. The answer is C. Activated protein C turns off the clotting cascade; in the absence of protein C, regulation of clotting is impaired, and clots can develop when not required. Mutations in any of the other answers listed would lead to excessive bleeding, as an essential component of the clotting cascade would be inactivated.
4. Classical hemophilia A results in an inability to directly activate which of the following factors?(A) Factor II(B) Factor IX(C) Factor X(D) Protein S(E) Protein C
4. The answer is C. Classical hemophilia is absence of Factor VIII, which is a necessary cofactor for the activation of Factor X by Factor IXa. Factor II is directly activated by Factor Xa, and Factor IX is directly activated by Factor XIa. Proteins C and S are directly activated by thrombin, Factor IIa.
5. Hemophilia B results in an inability to directly activate which of the following factors?(A) Factor II(B) Factor IX(C) Factor X(D) Protein S(E) Protein C
5. The answer is B. Hemophilia B is an inactivating mutation in Factor IX, such that Factor IXa cannot be formed. Factor XIa is formed, but its substrate, Factor IX, is defective, and a nonactive protein results.