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Pathology > Exam 1: Coagulation disorders > Flashcards

Exam 1: Coagulation disorders Flashcards

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
Q

some of the tissues/organs are highly susceptible to infarction due to

A

poor collateral circulation

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26
Q

do thrombi adhere to vessel walls?

A

yes, thrombi firmly adhere to vessel walls

27
Q

thrombi are composed primarily of platelets will be _____ in color

A

pale

28
Q

thrombi containing many RBC will often be _____

A

red

29
Q

____ thrombi will often be pale due to rate of flow, it prevents RBC from being incorporated into the thrombus

A

arterial

30
Q

thrombi in larger arteries may also have a _____ appearance, as multilayers of platelets, interspersed with fibrin, RBC, WBC, that get incorporated over time

A

laminated

31
Q

_____ 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

A

venous

32
Q

venous thrombi tend to be _____

A

gelatinous, soft, and glistening

33
Q

venous thrombi often occlude and _____ to the lumen of blood vessles

A

mold

34
Q

venous thrombi tend to extend _______ of th ethrombi as it continues to enlarge proximally when blood constituents come into contact with the thrombi

A

upstream

35
Q

post mortem clots will resemble ____ thrombi

A

venous

36
Q

post mortem clots firmly adhered to vessel walls?

A

no

37
Q

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

A

chicken fat

38
Q

post-mortem clots will also be devoid of

A

lesions on the vessel wall

39
Q

thrombi appearance on H&E

A

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
Q

what tissues are prone to ischemic necrosis

A

kidney, heart, and brain

41
Q

overtine, the affected area undergoes necrosis, swelling, and inflammation, the infarction will progressively become ____

A

paler; and eventually begin to shrink, as inflammation subsides and firbosis eventually replaces normal tissue

42
Q

acute infarcts on H&E

A

have hemorrhage, congestion, neutrophilic and/or fibrinous inflammation; loss of normal cell viability

43
Q

clinical signs depend on

A

the organ involved and amount of collateral circulation

44
Q

pulmonary thromboembolus signs

A

acute dyspnea

45
Q

gi signs

A

abdominal pain

46
Q

CNS signs

A

neurologic signs

47
Q

distal aorta signs

A

paresis, cool limbs, no femoral pulses

48
Q

common diseases associated with thrombosis include (but not limited to)

A

corticosteroid therapy/cushings
neoplasia
nephrotic syndrome
heartworm disease

49
Q

what is disseminated intravascular coagulation (DIC)

A

severe multifactorial disorder which occurs secondary to many primary disorders/proccesses

50
Q

these disorders/processes include

A

severe tissue trauma, disseminated bacteial infections, viral infections, neoplastic conditions, immune-mediated diseases

51
Q

DIC can have clinical bleeding if

A

clotting factors, inhibitors/promoters of clotting, and/or platelets have been depleted due to excessive clotting

52
Q

a primary disease process provides a potent trigger to activate widespread _____

A

clot formation in capillaries and small vessels

53
Q

this activation overwhelms the normal control mechanisms in place to

A

prevent/limit thrombus formation

54
Q

DIC results in widespread _____ formation in microvasculature

A

fibrin

55
Q

consequences are often

A

tisue ischemia and consumption of platelets, coagulation factors, natural inhibitors, and fibrinolytic factors

56
Q

ischemia often leads to

A

hypoxia or anoxia and localized or systemic metabolic acidosis

57
Q

if DIC is severe enough, it can result in

A

multiorgan failure and death

58
Q

DIC may often be recognized with

A

cpetichiation, ecchymosis, or bleeding

59
Q

underlying mechanisms associated with DIC

A

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
Q

gross DIC appearance

A

widespread, multifocal areas of petechia and ecchymosis in tissue
hemorrhage or hematomas may be present
a primary dz process may be observed

61
Q

DIC on H&E

A

microthrombi are hallmark
larger thrombi may be present
primary dz process

62
Q

clinical signs of DIC

A

petechia/ecchymosis
spontaneous bleeding/hematoma following venipuncture
organ dysfunction due to occlusion, anoxia
will not be specific

63
Q

common disorders associated with DIC

A 
massive trauma
spesis, septicemia, endotoxemia
neoplasia (vascular tumors)
necrotizing pancreatitis
IMHA
vasculitis
snake bite: VIC

Pathology (17 decks)

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