Exam 1: Coagulation disorders Flashcards
thrombosis
the formation of an inappropriate intravascular clot (fibrin, platelets,) on the wall or freely within the lumen
thrombus
actual intravascular clot
thrombosis occurs when
appropriate/normal fibrinolytic mechanisms fail to resolve clot properly during normal hemostatic events
ideal normal blood clot shouold be large enough to stop bleeding but not large enought to
occlude blood vessel
clot should be present only long enough to
allow healing of underlying vascular tissue
a thrombus can fragment or completely dislodge from primary site to form a
embolus or more appropreately termed thromboembolus
what is an embolism
the act of placing abnormal particulate matter into the circulation
particles within circulation are called
emboli
underlying causes of thrombotic disease are often ____
multifactorial
the three factors that greatly influence thrombus formation are termed Virchow’s triad and include
damage to endothelium
alteration in blood flow
hypercoagulability
damage to endothelium
provides focus for clot formation
alteration in blood flow
increased turbulence or increased statis
hypercoagulability of blood components
increased platelet activity
increased coagulation factor activity or increased coagulation factor activation
decreased natural inhibitors of coagulation
decreased antithrombin is well recognized in veterinary medicine
severe hepatic insufficiency (chronic or acute)
protein losing nephropathy and protein losing enteropathy
increased consumption (DIC)
decreased protein C
potential role for prognostic indicator; decreased in some equine colic and septicemia patients
what are the possible sequela if a thrombus or thrombi are formed
resolution secondary to fibrinolysis
organization plus/minus recanalization
enlargement/propagation leading to vascular obstruction
thromboembolism
resolution secondary to fibrinolysis (no long term effects)
complete dissolution following healing of underlying vessel wall
organization plus/minus recanalization
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
enlargement/propagation leading to vascular obstruction if involves artery
will cause ischemia unless collateral circulation exists
enlargement/propagation leading to vascular obstruction in vein
local edema, pain, swelling due to impaired drainage
what is the most common reason for an infarct
lodging of an embolus or thromboemolus
infarct
area of ischemic necrosis created by infarction usually well-demarcated
infarct usually due to
thrombotic or emobolic event
arterial obstruction but may occur with venous obstruction
development of an infarct is usually influenced by
type of vascular supply to tissue, rate of occlusion formation and sensitivity of tissue to oxygen deprivation
some of the tissues/organs are highly susceptible to infarction due to
poor collateral circulation
do thrombi adhere to vessel walls?
yes, thrombi firmly adhere to vessel walls
thrombi are composed primarily of platelets will be _____ in color
pale
thrombi containing many RBC will often be _____
red
____ thrombi will often be pale due to rate of flow, it prevents RBC from being incorporated into the thrombus
arterial
thrombi in larger arteries may also have a _____ appearance, as multilayers of platelets, interspersed with fibrin, RBC, WBC, that get incorporated over time
laminated
_____ 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
venous thrombi tend to be _____
gelatinous, soft, and glistening
venous thrombi often occlude and _____ to the lumen of blood vessles
mold
venous thrombi tend to extend _______ of th ethrombi as it continues to enlarge proximally when blood constituents come into contact with the thrombi
upstream
post mortem clots will resemble ____ thrombi
venous
post mortem clots firmly adhered to vessel walls?
no
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
post-mortem clots will also be devoid of
lesions on the vessel wall
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
what tissues are prone to ischemic necrosis
kidney, heart, and brain
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
acute infarcts on H&E
have hemorrhage, congestion, neutrophilic and/or fibrinous inflammation; loss of normal cell viability
clinical signs depend on
the organ involved and amount of collateral circulation
pulmonary thromboembolus signs
acute dyspnea
gi signs
abdominal pain
CNS signs
neurologic signs
distal aorta signs
paresis, cool limbs, no femoral pulses
common diseases associated with thrombosis include (but not limited to)
corticosteroid therapy/cushings
neoplasia
nephrotic syndrome
heartworm disease
what is disseminated intravascular coagulation (DIC)
severe multifactorial disorder which occurs secondary to many primary disorders/proccesses
these disorders/processes include
severe tissue trauma, disseminated bacteial infections, viral infections, neoplastic conditions, immune-mediated diseases
DIC can have clinical bleeding if
clotting factors, inhibitors/promoters of clotting, and/or platelets have been depleted due to excessive clotting
a primary disease process provides a potent trigger to activate widespread _____
clot formation in capillaries and small vessels
this activation overwhelms the normal control mechanisms in place to
prevent/limit thrombus formation
DIC results in widespread _____ formation in microvasculature
fibrin
consequences are often
tisue ischemia and consumption of platelets, coagulation factors, natural inhibitors, and fibrinolytic factors
ischemia often leads to
hypoxia or anoxia and localized or systemic metabolic acidosis
if DIC is severe enough, it can result in
multiorgan failure and death
DIC may often be recognized with
cpetichiation, ecchymosis, or bleeding
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
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
DIC on H&E
microthrombi are hallmark
larger thrombi may be present
primary dz process
clinical signs of DIC
petechia/ecchymosis
spontaneous bleeding/hematoma following venipuncture
organ dysfunction due to occlusion, anoxia
will not be specific
common disorders associated with DIC
massive trauma spesis, septicemia, endotoxemia neoplasia (vascular tumors) necrotizing pancreatitis IMHA vasculitis snake bite: VIC
