Exam 1: Coagulation disorders Flashcards

(63 cards)

1
Q

thrombosis

A

the formation of an inappropriate intravascular clot (fibrin, platelets,) on the wall or freely within the lumen

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2
Q

thrombus

A

actual intravascular clot

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3
Q

thrombosis occurs when

A

appropriate/normal fibrinolytic mechanisms fail to resolve clot properly during normal hemostatic events

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4
Q

ideal normal blood clot shouold be large enough to stop bleeding but not large enought to

A

occlude blood vessel

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5
Q

clot should be present only long enough to

A

allow healing of underlying vascular tissue

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6
Q

a thrombus can fragment or completely dislodge from primary site to form a

A

embolus or more appropreately termed thromboembolus

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7
Q

what is an embolism

A

the act of placing abnormal particulate matter into the circulation

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8
Q

particles within circulation are called

A

emboli

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9
Q

underlying causes of thrombotic disease are often ____

A

multifactorial

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10
Q

the three factors that greatly influence thrombus formation are termed Virchow’s triad and include

A

damage to endothelium
alteration in blood flow
hypercoagulability

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11
Q

damage to endothelium

A

provides focus for clot formation

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12
Q

alteration in blood flow

A

increased turbulence or increased statis

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13
Q

hypercoagulability of blood components

A

increased platelet activity
increased coagulation factor activity or increased coagulation factor activation
decreased natural inhibitors of coagulation

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14
Q

decreased antithrombin is well recognized in veterinary medicine

A

severe hepatic insufficiency (chronic or acute)
protein losing nephropathy and protein losing enteropathy
increased consumption (DIC)

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15
Q

decreased protein C

A

potential role for prognostic indicator; decreased in some equine colic and septicemia patients

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16
Q

what are the possible sequela if a thrombus or thrombi are formed

A

resolution secondary to fibrinolysis
organization plus/minus recanalization
enlargement/propagation leading to vascular obstruction
thromboembolism

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17
Q

resolution secondary to fibrinolysis (no long term effects)

A

complete dissolution following healing of underlying vessel wall

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18
Q

organization plus/minus recanalization

A

in-growth of fibroblasts, endothelial cells and smooth muscle cells
blood flow will renew as capillaries anastomose
will gradually decrease in size as connective tissue contracts

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19
Q

enlargement/propagation leading to vascular obstruction if involves artery

A

will cause ischemia unless collateral circulation exists

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20
Q

enlargement/propagation leading to vascular obstruction in vein

A

local edema, pain, swelling due to impaired drainage

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21
Q

what is the most common reason for an infarct

A

lodging of an embolus or thromboemolus

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22
Q

infarct

A

area of ischemic necrosis created by infarction usually well-demarcated

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23
Q

infarct usually due to

A

thrombotic or emobolic event

arterial obstruction but may occur with venous obstruction

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24
Q

development of an infarct is usually influenced by

A

type of vascular supply to tissue, rate of occlusion formation and sensitivity of tissue to oxygen deprivation

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25
some of the tissues/organs are highly susceptible to infarction due to
poor collateral circulation
26
do thrombi adhere to vessel walls?
yes, thrombi firmly adhere to vessel walls
27
thrombi are composed primarily of platelets will be _____ in color
pale
28
thrombi containing many RBC will often be _____
red
29
____ thrombi will often be pale due to rate of flow, it prevents RBC from being incorporated into the thrombus
arterial
30
thrombi in larger arteries may also have a _____ appearance, as multilayers of platelets, interspersed with fibrin, RBC, WBC, that get incorporated over time
laminated
31
_____ thrombi will often be dark red in appearance due to the incorporation of erythrocytes into the thrombus due to the lower blood flow in these vessels
venous
32
venous thrombi tend to be _____
gelatinous, soft, and glistening
33
venous thrombi often occlude and _____ to the lumen of blood vessles
mold
34
venous thrombi tend to extend _______ of th ethrombi as it continues to enlarge proximally when blood constituents come into contact with the thrombi
upstream
35
post mortem clots will resemble ____ thrombi
venous
36
post mortem clots firmly adhered to vessel walls?
no
37
in the heart or large vessels, post mortem clots will often have a _____ appearance, as the RBC will sediment to the dependent side of the clot
chicken fat
38
post-mortem clots will also be devoid of
lesions on the vessel wall
39
thrombi appearance on H&E
generally intraluminal eosinophilic, smooth to laminar material partially or completely occludes the vessel; adhearing to tunica interna; RBC, WBC, fibroblasts and endothelial cells will be noted
40
what tissues are prone to ischemic necrosis
kidney, heart, and brain
41
overtine, the affected area undergoes necrosis, swelling, and inflammation, the infarction will progressively become ____
paler; and eventually begin to shrink, as inflammation subsides and firbosis eventually replaces normal tissue
42
acute infarcts on H&E
have hemorrhage, congestion, neutrophilic and/or fibrinous inflammation; loss of normal cell viability
43
clinical signs depend on
the organ involved and amount of collateral circulation
44
pulmonary thromboembolus signs
acute dyspnea
45
gi signs
abdominal pain
46
CNS signs
neurologic signs
47
distal aorta signs
paresis, cool limbs, no femoral pulses
48
common diseases associated with thrombosis include (but not limited to)
corticosteroid therapy/cushings neoplasia nephrotic syndrome heartworm disease
49
what is disseminated intravascular coagulation (DIC)
severe multifactorial disorder which occurs secondary to many primary disorders/proccesses
50
these disorders/processes include
severe tissue trauma, disseminated bacteial infections, viral infections, neoplastic conditions, immune-mediated diseases
51
DIC can have clinical bleeding if
clotting factors, inhibitors/promoters of clotting, and/or platelets have been depleted due to excessive clotting
52
a primary disease process provides a potent trigger to activate widespread _____
clot formation in capillaries and small vessels
53
this activation overwhelms the normal control mechanisms in place to
prevent/limit thrombus formation
54
DIC results in widespread _____ formation in microvasculature
fibrin
55
consequences are often
tisue ischemia and consumption of platelets, coagulation factors, natural inhibitors, and fibrinolytic factors
56
ischemia often leads to
hypoxia or anoxia and localized or systemic metabolic acidosis
57
if DIC is severe enough, it can result in
multiorgan failure and death
58
DIC may often be recognized with
cpetichiation, ecchymosis, or bleeding
59
underlying mechanisms associated with DIC
stagnant blood flow endothelial damage release of large quantitis of tissue factors release of particulate matter (phospholipids, microparticles) release of proteolytic enzymes into blood decreased clearance of activated coagulation factors consumption of inhibitors of coagulation
60
gross DIC appearance
widespread, multifocal areas of petechia and ecchymosis in tissue hemorrhage or hematomas may be present a primary dz process may be observed
61
DIC on H&E
microthrombi are hallmark larger thrombi may be present primary dz process
62
clinical signs of DIC
petechia/ecchymosis spontaneous bleeding/hematoma following venipuncture organ dysfunction due to occlusion, anoxia will not be specific
63
common disorders associated with DIC
``` massive trauma spesis, septicemia, endotoxemia neoplasia (vascular tumors) necrotizing pancreatitis IMHA vasculitis snake bite: VIC ```