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62 Cards in this Set
- Front
- Back
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what are the control mechanisms in hemostasis?
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dilution of clotting factor, clearance of activated clotting factors, protease inhibitors (antithrombin III), clot retraction, fibrinolytic system, counterbalancing fibrinolysis
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what are dilution of clotting factor, clearance of activated clotting factors, protease inhibitors (antithrombin III), clot retraction, fibrinolytic system, counterbalancing fibrinolysis
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control mechanisms in hemostasis
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how does the dilution of clotting factor affect hemostasis?
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most significant on arterial side; sweeps away platelets
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how does clearance of activated clotting factors affect hemostasis?
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occurs when flow of blood away from site, handled by liver and MPs
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how do antithrombins affect hemostasis?
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these protease inhibitors are activated by binding to heparin or heparin-like molecules on endothelial cells; inhibit thrombin and other serine proteases (IXa, Xa, XIz, XIIa)
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how does clot retraction affect hemostasis?
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allow reflow of clot if sufficiently reduced in size
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how does the fibrinolytic system affect hemostasis?
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chews up clot, forms fibrin degradation products (FDPs)
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what are the processes of the fibrinolytic system?
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plasminogen activators convert plasminogen to plasmin which then degrades fibrin to FDPs which inhibit clotting
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what does the Fibrinolytic system do?
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it converts plasminogen to plasmin via 'plasminogen activators'
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name plasminogen activators?
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kallikrein generated by Hageman factor, products of microorganisms (streptokinase), tissue activators (tPA), leukocytic activators, biological fluids, others
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kallikrein generated by Hageman factor, products of microorganisms (streptokinase), tissue activators (tPA), leukocytic activators, biological fluids, others are what?
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plasminogen activators
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what does plasmin convert fibrin to in the fibrinolytic system?
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fibrin degradation products (FDPs)
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what do FDP's do?
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inhibit clotting by inhibiting fibrin polymerization, inhibit platelet reactions, involved in the pathogenesis of disseminated intravascular coagulation (DIC)
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what are D-dimers?
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new measure of FDP's
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what is a measure of FDP's?
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D-dimers
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what are D-dimers from?
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it is a breakdown product of fibrin mesh, from factor XIII
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what counterbalances fibrinolysis in hemostasis?
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inhibitors of fibrinolysis: plasminogen activator inhibitors & alpha-2 antiplasmin
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what do plasminogen activator inhibitors do?
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prevent fibrin binding to tPA
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what do alpha-2 antiplasmins do?
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inhibit binding of fibrin to plasmin
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what interupts the balance between plasminogen activator inhibitors and alpha-2 antiplasmins?
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interrupted by severe infections (IL-1/TNF) which augments tissue factor and inhibits fibrinolysis which favors thrombosis
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what does DIC stand for?
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disseminated intravascular coagulation
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how can DIC be describes as (one word)?
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paradox
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what is another term for DIC?
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consumptive coagulopathy
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what is the DIC paradox?
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widespread formation of fibrin and platelet rich thrombi in microcirculation; syndrome, not a disease process
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what occurs in DIC after consumption of platelets and clotting factors?
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consumption of platelets and clotting factors that cause widespread microthrombi and tissue infarction cause hemorrhages from small vessels
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what occurs in DIC with consumptive coagulopathy?
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bleeding in the face of widespread thrombosis
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what is thrombasthenia?
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deficiency of GpIIb-IIIa resulting in a severe bleeding disorder
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what is Von Willebrand's disease?
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defect in vWF (dobermans) causes defective platelet adhesion which increases bleeding time
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define thrombosis?
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formation of a solid mass from the constituents of blood within the cardiovascular system of a living animal, inappropriate hemostasis
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thrombosis is a pathological manifestation of what?
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blood coagulation
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the initiation of thrombosis can be explained by what?
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Virchow's triad
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what are the components of Virchow's triad?
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endothelial injury, alterations in normal blood flow (rheological), hypercoagulability of blood
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what alterations in normal blood flow (rheological) exist in Virchow's triad?
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stasis & turbulence
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stasis and turbulence are qualities of what in Virchow's triad?
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alterations in normal blood flow
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what do alterations in stasis and turbulance do?
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disrupt laminar flow and not allow thrombogenic factors to be swept away
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what are examples of endothelial damage that can cause turbulance?
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mass impinging on vessel walls, rigid heart valves, atherosclerotic plaques (subendothelial plaques), arterial aneurysm, verminous arteritis
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what does a mass impinging on a vessel wall cause
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turbulent flow and platelet buildup
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what do rigid heart valves cause?
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turbulence, eddy currents, and stasis resulting in sediment plaques
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what do atherosclerotic plagque (subendothelial fat) cause?
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turbulent flow and endothelial injury
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what do arterial aneurysms cause?
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sedimentation and endothelial disruption
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what do verminous arteritis cause?
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roughening of cranial mesenteric artery (from Strongylus vulgaris)
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what are examples of endothelial damage that can cause stasis?
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spasm of vessel and deep vein thrombosis
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what do spasms of vessels cause?
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platelet sediment
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what causes Deep vein thrombosis?
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long periods of inactivity
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what alterations in hypercoagulability of blood exist in Virchow's triad?
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increased numbers of platelets, elevated fibrinogen (or other clotting factors), decreased antithrombin III (renal dz/nephrotic syndrome), decreased activity of fibrinolytic system
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elevated fibrinogen, decreased antithrombin III, decreased activity of fibrinolytic system are features of what in Virchow's triad?
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hypercoagulability of blood
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endothelial injury, alterations in normal blood flow (rheological), hypercoagulability of blood are components of what?
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Virchow's triad
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what are the potential morphologies of thrombosis?
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arterial (pale) thrombi, venous (red) thrombi, vegetations, postmortem clots
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what occurs to form arterial (pale) thrombi?
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rapid blood flow washes away cells
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what is the gross morphology of areterial (pale) thrombi?
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dry, friable gray masses, alternating layers of fibrin and platelets with scant RBDs
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where are arterial (pale) thrombi found?
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attached to site of endothelial damage (mural thrombi) or occulsive (ex cerebral artery.)
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what occurs to form venous (red) thrombi?
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slower blood flow causes more cellular constituents/platelets entrapped
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what is the gross morphology of venous (red) thrombi?
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more gelatinous, moist, red, but closely resemble postmortem clots except slightly firmer, may have some fibrin layers, more firmly attached to endothelium at point of primary origin
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where are venous (red) thrombi found?
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rarely mural, more commonly occlusive
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what are vegetations?
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thrombi that build up on heart valves
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what is the gross morphology of vegetations?
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look like cauliflower with rough or plaque-like appearance
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what occurs to form vegetations?
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sites of endothelial injury due to bacteremia/other antigens resulting in vegetative valvular endocarditis
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what do postmortem clots resemble?
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venous thrombi
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how do we distinguish postmortem clots from venous thrombi?
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postmortem clots easily separate from intima of vessels, not layered with even coloring
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what are the two forms of postmortem clots?
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currant jelly clot & chicken fat clot
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what is the gross morphology of currant jelly clot?
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dark red, glistening smooth surface, consistency of gelatine
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what is the gross morphology of chicken fat clot?
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red cells sediment before clot forms while the upper part is yellow plasma
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