1what are the stages of coagulation
- primary hemostasis
- clot formation
- secondary hemostasis
- fibronolysis
- tertiary hemostasis
2what is primary hemostasis
- injury factors signal to the body that a clot needs to form, vessels constrict
- coagulation factors begin making fibrin to stabilize platelet plug
- injury to a blood vessel, vessel constriction, then platelet accumulation
- clot breaks down after wound heals
3how is a chemically stable fibrin clot made
- clot is made in the liver and sent to the injury site
- fibrin strands react individually and bridge the gap
- series of related, enzyme-mediated reactions reinforce the platelet plug
- area of injury secretes factors that form fibrin plug
4zymogens are:
- signaling molecules released when vessels are injured
- active coag factors
- inactive coag factors
- released during secondary hemostasis
5end result of activated zymogens
- initiation of primary hemostasis
- fibrin clot degradation
- blood vessel healing
- fibrin clot formation
6where are zymogens found
- liver
- lymphatic fluid
- blood
- bone marrow
7main site of coag factor production
- liver
- pancreas
- circulating blood
- bone marrow
8factor I
- fibrinogen
- proaccelerin
- tissue factor
- prothrombin
9factor II
- calcium
- prothrombin
- proaccelerin
- von willebrand factor
10factor III
- stuart factor
- prothrombin
- tissue factor
- fibrinogen
11factor IV
- fibrin-stabilizing factor
- calcium (Ca ++)
- fibrinogen
- antihemophilic factor
12factor V
- stuart factor
- calcium (Ca ++)
- proaccelerin
- hagemaan factor
13factor VII
- antihemophilic factor
- proconvertin (stable factor)
- stuart factor
- von willebrand factor
14factor VIII
- calcium (Ca ++)
- fletcher factor
- hageman factor (contact factor)
- antihemophilic factor
15vWf
- von willebrand factor
- proaccelerin
- fibrinogen
- stuart factor
16factor IX
- antihemophilic factor
- plasma thromboplastin component (PTC)
- proconvertin
- fibrin-stabilizing factor
17factor X
- stuart factor
- fletcher factor
- von willebrand factor
- hageman factor
18factor XI
- plasma thromboplastin antecedent (PTA)
- plasma thromboplastin component (PTC)
- fitzgerald factor
- fletcher factor
19factor XII
- fletcher factor
- hageman factor (contact factor)
- plasma thromboplastin component (PTC)
- fibrin-stabilizing factor
20factor XIII
- fibrin-stabilizing factor
- tissue factor
- hageman factor
- antihemophilic factor
21HK (high molecular weight kiminogen)
- proconvertin
- fitzgerald factor
- fletcher factor
- proaccelerin
22PK (prekallikrein)
- von willebrand factor
- stuart factor
- fitzgerald factor
- fletcher factor
23which of the following is NOT a group of coag factors
- antihemophilic group
- fibrinogen group
- contact group
- prothrombin group
24fibrinogen group includes factors
- I, VI, VIII, XII
- I, V, VIII, XIII
- I, V, VII, XIII
- II, V, VIII, XII
25all factors in this group are consumed during the process of coag
- prothrombin
- proconvertin
- contact
- fibrinogen
26where can the factors of the fibrinogen group be found in the body
- present in plasma, absent in serum
- only found in the liver
- present in both plasma and serum
- absent in plasma, present in serum
27which factors make up the prothrombin group
- II, VI, XII, XIII
- II, VII, IX, X
- III, VII, IX, X
- I, V, VII, VIII
28factors of this group (aside from factor II) are not consumed during the process of coag
- contact
- proaccelerin
- prothrombin
- fibrinogen
29which member of the prothrombin group is found only in plasma, unlike the rest which are found in both plasma and serum
- factor III
- factor II
- factor X
- factor VII
30which vitamin is required for the synthesis of factors in the prothrombin group
31why is vit K required for the synthesis of factors in the prothrombin group
- activates factors when an injury occurs
- prevents factors from binding calcium
- allows for clot formation when other groups are unavailable or dysfunctional
- allows factors to bind calcium
32why is it important for calcium to bind to factors in the prothrombin group
- binding is required to activate the factors
- binding signals to factors in other families to start working
- binding causes a conformational change that allows them to interact
- binding helps fibrin strands come together and form a plug
33which factors are in the contact group
- XI, XII, PK, vWf
- X, XIII, PK, HK
- VII, VIII, X, XIII
- XI, XII, PK, HK
34factors of this group are not consumed during coag
- contact
- thromboplastin
- prothrombin
- fibrinogen
35where are factors in the contact group found
- present in plasma and serum
- only factor XII is found in plasma, the rest are found in serum
- present in plasma, absent in serum
- absent in plasma, present in serum
36what is a requirement for the activation of factors in the contact group
- reception of signaling molecule from the liver
- binding with calcium
- contact with a surface
- binding with vit K
37the ______ and _______ pathways come together in the _______ pathway
- internal, external, vascular
- intrinsic, extrinsic, vascular
- intrinsic, extrinsic, common
- hepatic, extrinsic, common
38which pathway is necessary for large amounts of fibrin
- common
- all of the above
- extrinsic
- intrinsic
39which substance not normally present in blood serves as the start of the extrinsic pathway
- fibrinogen
- vit K
- von willebrand factor
- tissue factor/tissue thromboplastin
40how does tissue factor/tissue thromboplastin serve as the start of the extrinsic pathway
- it enters the vascular endothelium when a clot needs to be dissolved
- it's a glycoprotein that's only expressed in the presence of vit K
- it's exposed to the bloodstream when a blood vessel is injured
- it stops the process of the intrinsic pathway
41tissue factor/thromboplastin combines with ________ to begin the extrinsic pathway
- vit K
- factor XII
- fibrinogen
- factor VII
42what is required for the activation of the serine protease factor VIIa
- serine cleavage of zymogen factor V
- serine cleavage of zymogen factor VII
- binding to calcium
- interaction with fibrinogen
43at what point during the coag process is the clot formed
- end of the common pathway
- during the transition from the extrinsic to common pathway
- end of the extrinsic pathway
- end of the intrinsic pathway
44what are the components that make up the extrinsic Xase complex
- factor VIIa, TF, calcium
- von willebrand factor, TF, vit K
- factor VIIa, TF, vit K
- factor VIIa, fibrinogen, calcium
45exposure to negatively charged foreign subtstances such as collagen or subendothelium can activate ______
- factor XII -> factor XIIa
- factor HK -> PK
- factor VIII -> factor VIIIa
- factor XII -> factor XIII
46describe the process of secondary hemostasis
- platelets aggregate at the site of injury
- coag factors form fibrin that stabilize the plt plug
- coag factors initiate the intrinsic pathway
- blood vessel injury signals to circulating factors that a clot must be formed
47which of the following is not a step in the process of primary hemostasis
- platelet shape change
- platelet accumulation
- platelet secretion of granules
- platelet activation
- platelet aggregation
- platelet adhesion
48which factors are considered labile?
- V, VII
- V, VIII
- VIII, IX
- VII, VIII
49which factors are cofactors?
- III, V, VIII
- V, VIII, XII
- II, III, IX
- III, VI, VII
50why is the INR important
- it's used to correct for differences in reagents/instruments in PT testing
- it corrects for differences in clotting time for patients on anticoagulants
- it's used to calculate accurate aPTT results
- none of the above
51reference range for platelet count
- 150-450 x 10^6 /microliter
- 150-450 x 10^3 /microliter
- 150-450 x 10^9 /microliter
- 150-450 x 10^5 /microliter
52what is the purpose of vasoconstriction following an injury?
- recuit factors for the extrinsic pathway
- minimizes blood flow to wound area
- allow blood to come into contact with collagen in the subendothelium
- trigger local release of epinephrine and a myogenic spasm
53what hormone is secreted by endothelial cells that serves as a vasoconstrictor
- thromboplastin
- endothelin
- epinephrine
- collagen
54what is the difference between intact and damaged endothelial cells during coagulation
- intact, negatively charged cells repel platelets and proteins
- injured, negatively charged cells repel platelets and proteins
- intact, positively charged cells repel platelets and proteins
- injured, positively charged cells repel platelets and proteins
55what cells immediately begin forming a plug to stop the bleeding caused by an injury
- intact endothelial cells
- platelets
- red blood cells
- injured endothelial cells
56what is platelet adhesion
- platelets extends its membrane into pseudopods to increase contact with other platelets
- vWf is released into plasma, binds to GPIb, and attaches platelets to collagen in the blood vessel wall
- platelets generate agonists thrombin and ADP to help bind platelets to colagen in the vessel wall
- collagen attaches to GPIb receptor to recruit vWf
57where is vWf made and what does it do
- liver/megakaryocytes - activates granule release
- bone marrow/megakaryocytes - binds to collagen
- endothelial cells/liver - binds agonist TXA2
- edothelial cells/megakaryocytes - binds GPIb receptor
58what triggers platelet activation
- binding of vWf to GPIb
- adhesion of platelets to collagen
- synthesis of myosin
- release of vWf from endothelial cells
59what is an agonist
- agent that induces fibrolysis
- agent that induces platelet activation
- molecule that binds GPIb receptor
- molecule that recruits activates platelets to plug
60what are the 2 types of agonists
- platelet derived, endothelial derived
- surface binding, intracellular binding
- platelet derived, non platelet derived
- positive, negative
61what is the purpose of platelet shape change
- allow cytoskeleton to grow
- increase surface area for more vWf binding
- pseudopods decrease the chances of platelets coming into contact
- pseudopods increase the chances of platelets coming into contact
62what is secreted from platelets following their shape change?
- light and dense granules
- primary and secondary graunles
- alpha and beta granules
- alpha and dense granules
63which are commonly found in alpha granules
- thrombospondin, vWf, PDGF
- thrombospondin, collagen, ADP
- vWF, ADP, calcium
- ADP, calcium, serotonin
64which are commonly found in dense granules
- ADP, potassium, serotonin
- ADP, calcium, serotonin
- PDGF, thrombospondin, vWf
- vWf, calcium, dopamine
65what is platelet aggregation
- attachment of platelets to one another
- attachment of platelets to the vessel wall
- binding of vWf to GPIb
- platelet pseudopods interlink
66why do platelets secrete granules
- granules participate in immune responses
- granules release activated coag factors
- they help the platelet attach to the vessel wall
- their contents attract and activate new platelets
67how is fibrin stabilizing factor (FXIII) activated
- thrombin cleaves a peptide to form FXIIIa
- prothrombin cleaves a peptide to form YXIIIa
- binding with TF/FIII after a vessel is injured
- fibrin crosslinks molecules of FXIII
68what is the function of activated FXIII (FXIIIa)
- it creates crosslinked fibrin
- it converts prothrombin to thrombin
- it converts fibrinogen to fibrin
- it joins the prothrombinase complex
69what PT/aPTT results would you expect from an underfilled blue top
- both are falsely prolonged
- both are falsely decreased
- PT is prolonged, aPTT is normal
- PT is normal, aPTTT is decreased
70what is NOT tested by thromboelastography
71what receptor participates in platelet aggregation but not paltelet adhesion
72what is the activator for the PT test
- tissue factor (III)
- FV
- FVIII
- calcium chloride