EMBOLISM, ISCHEMIA AND INFARCTION
|Now that you have
an understanding of normal hemostasis we will discuss diseased states
as a result of abnormal hemostasis, and obstruction of blood flow: namely,
thrombosis, embolism, ischemia and infarction.
Thrombosis is the
abnormal formation of a blood clot within the vasculature of a living
animal. There are 3 major causes for thrombosis:
in normal blood flow
of the blood.
Thrombosis can result
from any one or any combination of the above.
|Remember from the
unit on hemostasis that the endothelial cells have several anti-thrombotic
properties. For example, endothelial cells secrete PGI2 which
inhibits platelet aggregation. Endothelial release of nitric
oxide causes vasodilation and inhibits platelet adhesion and
aggregation. Also, endothelial cells elaborate protein C and
endothelial surfaces are covered with heparin-like molecules that
promote the activity of anti-thrombin III.
|The triangle here is referred to as Virchow's triad. You don't have to remember that. But you do have to remember that any time there is a thrombus, it has to be ONE (or more) of the THREE parts of the triad. So, please, guarantee yourself some points on the exam and some acumen in the clinic by always thinking of these three causes when there is a thrombus present.
|In addition to the
anti-thrombotic activities of endothelial cells, damage can result in
release of tissue thromboplastin (also known as tissue factor) and exposure of the sub-endothelial
vascular collagen to platelets and clotting factors. During inflammation,
cytokines (ie. IL-1 and TNF-alpha), can induce endothelial cells to synthesize
and release tissue factor.
adhere to the exposed sub-endothelial collagen where the endothelium
has been lost.
via von Willebrand's factor (vWF) and tissue factor is released
by adjacent damaged tissue activating the coagulation cascade.
Loss or injury
to endothelium results in decreased PGI2 and nitric
oxide which normally inhibits platelet aggregation and causes
A2 (TXA2) from platelets causes vasoconstriction
and in conjunction with ADP stimulates aggregation.
|Here are some examples
of thrombosis due to endothelial cell damage:
||We are looking
at the aortic valves of an older dog. Note the cauliflower-like
vegetative growths on the valves. How
did these THROMBI form?
repeated venipuncture, catheters, or repeated injections with caustic
medications results in endothelial damage and thrombosis. This
horse died. Wanna
Jugular thrombosis is often associated with repeated injections
or with indwelling catheters.
||From a horse with recurring colic - this is the
aorta running across the top of the photograph and the cranial
mesenteric artery projecting below. Holy mackerel - the cranial
mesenteric artery is all plugged with a big old thrombus. How
the heck did this happen and what might be the result?