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General Pathology > Vascular Disorders and Thrombosis II > Flashcards

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
Q

what is plasmin derived from?

A

circulating plasminogen

26
Q

what are the two major functions of plasmin?

A

fibrinolysis
inhibition of fibrin polymerization

27
Q

what is a thrombus?

A

aggregate of platelets, fibrin, and blood cells
temporary patch
inappropriately large or persistent blood clot

28
Q

what is thrombosis?

A

formation of a pathologic thrombus

29
Q

what is an embolus?

A

thrombus or thrombus fragment is moved from its origin to a distant vessel

30
Q

what are the factors leading to pathologic thrombosis?

A

endothelial injury
abnormal blood flow
hypercoagulable state

31
Q

how can blood flow be altered in virchow’s triad?

A

stasis
turbulence

32
Q

what can lead to hypercoagulability in virchow’s triad?

A

inflammation
glomerular disease
protein losing enteropathy
liver disease
endocrine disorders
neoplasia

33
Q

what are the outcomes of thrombosis?

A

hypoxia
ischemia
infarction/infarct

34
Q

what makes up a reperfusion injury?

A

formation reactive oxygen species
inflammation/mediators

35
Q

what does the color of an infarction depend on?

A

whether offending thrombus arterial or venous
types of tissue
duration infarct

36
Q

what can an embolus be?

A

detached thrombus (most frequent)
fat or bone marrow
gas bubble
tumor fragment
bacterial colonies
foreign objects

37
Q

what may larger, chronic thrombi be replaced by?

A

granulation tissue, fibrosis +/- mineralization
recanalization

38
Q

what does recanalization entain?

A

growth of new endothelium
formation of capillary channels
reinstitution of small amount of blood flow around/through thrombus

39
Q

what is an antemortem thrombus like?

A

firm, adhered to vessel wall
red to tan, dull, often granular

40
Q

what is a postmortem clot like?

A

soft, gelatinous, loosely or not adhered to vessel wall
deep red and smooth often, can be tan/yellow if red cells settle out

41
Q

how can you distinguish an arterial thrombus from a venous one?

A

arterial is often more pale
see gross or microscopic lamellations (lines of Zahn)

42
Q

how can you tell a thrombus is venous instead of arterial?

A

more red
less firm
should have attachment point on vessel wall
similar in appearance to postmortem clot

43
Q

how does hypertrophic cardiomyopathy in cats lead to a saddle thrombus (embolism in distal abdominal aorta)?

A

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
Q

where is the defect in primary hemostatic disorders?

A

platelet arm of coagulation

45
Q

what are the characteristics of von Willebrand disease?

A

decreased or absent von Willebrand’s Factor
platelet numbers and function are normal
reduces ability of platelets to bind to subendothelial collagen

46
Q

what are the characteristics of hemostatic disorders?

A

hematomas
cavitary hemorrhage
delayed bleeding from venipuncture sites

47
Q

is liver disease with loss of hepatic parenchyma and example of secondary or primary hemostatic disorders?

A

secondary hemostatic disorders

48
Q

true/false: a patient with liver disease with loss of hepatic parenchyma is at risk for hyper- and hypocoagulabilty

A

true

49
Q

what do vitamin K antagonist rodenticides inhibit?

A

factors II, VII, IX, X from binding calcium and phospholipid surface

50
Q

what happens in disseminated intravascular coagulation with clotting and clotting factors?

A

widespread activation of coagulation in small vessels
massive consumption of platelets and clotting factors

51
Q

what is hypoxanthine?

A

reacts with oxygen to form free radicals in reperfusion injury

General Pathology (9 decks)

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