Vascular Disorders and Thrombosis II Flashcards

1
Q

what are the major players in hemostasis?

A

endothelium and underlying matrix
platelets
circulating factors

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2
Q

what do prostacyclin and nitric oxide do with thrombosis?

A

inhibit platelet activation, adhesion, and aggregation
vasodilate

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3
Q

does ADPase promote thrombosis or prevent it?

A

prevents it: degrades pro-thrombotic ADP

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4
Q

what does tissue plasminogen activator do?

A

activates plasmin to digest fibrin

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5
Q

what are the membrane associated factors of endothelium that prevent thrombus?

A

thrombomodulin and circulating proteins C and S
heparin-like molecules and circulating antithrombin III
tissue factor pathway inhibitor

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6
Q

what does endothelin do?

A

vasoconstricts

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7
Q

what does von Willebrand Factor do?

A

enhances platelet binding to collagen

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8
Q

what does platelet activating factor do?

A

recruits and activates platelets

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9
Q

what does tissue factor (factor III) do?

A

initiates extrinsic coagulation pathway

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10
Q

what do plasminogen activator inhibitors do?

A

inhibit fibrinolysis

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11
Q

what do platelets secrete to promote aggregation?

A

calcium
ADP- also activation
thromboxane A2- vasoconstricts as well

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12
Q

what is the primary producer of most circulating clotting and anticoagulant factors?

A

liver

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13
Q

what clotting factors produced by the liver are vitamin K-dependent?

A

II, VII, IX, X
protein C and protein S

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14
Q

what is the primary initiator of the coagulation cascade in vivo?

A

extrinsic pathway: activated by exposure of Tissue Factor (factor III) to factor VII in circulation

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15
Q

what is the primary amplifier of the coagulation cascade in vivo?

A

intrinsic pathway: activated by negatively-charged substances, collagen, inflammatory pathways

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16
Q

what factors are involved in the intrinsic pathway for the coagulation cascade?

A

factors XII, XI, IX, VIII

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17
Q

when do the extrinsic and intrinsic pathways merge?

A

activation of factor X: factor X and V= prothrombinase complex

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18
Q

what is the ratio of blood to anticoagulant for a coagulation test?

A

9:1

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19
Q

what is the initiation of the cell-based model of coagulation?

A

circulating VIIa binds tissue factor on surface damaged endothelial cells
factor Xa and a small amount of thrombin are produced

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20
Q

how does thrombin amplify coagulation?

A

activates platelets, cleaves von Willebrand’s Factor-VIII complex, and activates factors V, VIII, XI

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21
Q

what do activated coagulation factors aggregating on activated platelets lead to?

A

production abundant Xa

22
Q

what do Xa and Va produce?

A

abundant thrombin

23
Q

what inhibits fibrinolysis?

A

alpha-2 antiplasmin
plasminogen activator inhibitor-1

24
Q

what activates plasmin for fibrinolysis?

A

tissue plasminogen activator
urokinase-type plasminogen activator

25
what is plasmin derived from?
circulating plasminogen
26
what are the two major functions of plasmin?
fibrinolysis inhibition of fibrin polymerization
27
what is a thrombus?
aggregate of platelets, fibrin, and blood cells temporary patch inappropriately large or persistent blood clot
28
what is thrombosis?
formation of a pathologic thrombus
29
what is an embolus?
thrombus or thrombus fragment is moved from its origin to a distant vessel
30
what are the factors leading to pathologic thrombosis?
endothelial injury abnormal blood flow hypercoagulable state
31
how can blood flow be altered in virchow's triad?
stasis turbulence
32
what can lead to hypercoagulability in virchow's triad?
inflammation glomerular disease protein losing enteropathy liver disease endocrine disorders neoplasia
33
what are the outcomes of thrombosis?
hypoxia ischemia infarction/infarct
34
what makes up a reperfusion injury?
formation reactive oxygen species inflammation/mediators
35
what does the color of an infarction depend on?
whether offending thrombus arterial or venous types of tissue duration infarct
36
what can an embolus be?
detached thrombus (most frequent) fat or bone marrow gas bubble tumor fragment bacterial colonies foreign objects
37
what may larger, chronic thrombi be replaced by?
granulation tissue, fibrosis +/- mineralization recanalization
38
what does recanalization entain?
growth of new endothelium formation of capillary channels reinstitution of small amount of blood flow around/through thrombus
39
what is an antemortem thrombus like?
firm, adhered to vessel wall red to tan, dull, often granular
40
what is a postmortem clot like?
soft, gelatinous, loosely or not adhered to vessel wall deep red and smooth often, can be tan/yellow if red cells settle out
41
how can you distinguish an arterial thrombus from a venous one?
arterial is often more pale see gross or microscopic lamellations (lines of Zahn)
42
how can you tell a thrombus is venous instead of arterial?
more red less firm should have attachment point on vessel wall similar in appearance to postmortem clot
43
how does hypertrophic cardiomyopathy in cats lead to a saddle thrombus (embolism in distal abdominal aorta)?
left ventricle fills poorly, so left atrium is backed up left atrium remodels by dilation and local endothelial damage with stretching stasis and endothelial injury leads to clot in left atrium dislodges
44
where is the defect in primary hemostatic disorders?
platelet arm of coagulation
45
what are the characteristics of von Willebrand disease?
decreased or absent von Willebrand's Factor platelet numbers and function are normal reduces ability of platelets to bind to subendothelial collagen
46
what are the characteristics of hemostatic disorders?
hematomas cavitary hemorrhage delayed bleeding from venipuncture sites
47
is liver disease with loss of hepatic parenchyma and example of secondary or primary hemostatic disorders?
secondary hemostatic disorders
48
true/false: a patient with liver disease with loss of hepatic parenchyma is at risk for hyper- and hypocoagulabilty
true
49
what do vitamin K antagonist rodenticides inhibit?
factors II, VII, IX, X from binding calcium and phospholipid surface
50
what happens in disseminated intravascular coagulation with clotting and clotting factors?
widespread activation of coagulation in small vessels massive consumption of platelets and clotting factors
51
what is hypoxanthine?
reacts with oxygen to form free radicals in reperfusion injury