Biomedical Engineering Reference
In-Depth Information
circulated in the blood and are responsible for hemostasis, which leads to the release
of thread fibers to enable blood clotting.
Low quantity of platelets, which is a condition known as thrombocytopenia, re-
sults in excessive bleeding. On the other hand, high quantity of platelets can cause
thrombocytosis results in blood clotin which blocks blood vessels and increase the
risk of stroke, myocardial infarction (heart attack), or pulmonary embolism. If the
carotid arteries are blocked, then cerebral thrombosis occurs. This abnormality is
known as thrombocytopathy.
2.3
Disease of the Cardiovascular System
2.3.1
Atherosclerosis
Atherosclerosis is a pathological process that takes place in the major arteries and
is the underlying cause of heart attacks, stroke and peripheral artery disease. In an
atherosclerotic artery, the lumen is narrowed and the arterial wall is stiffened by
the build-up of fatty plaque beneath the endothelium (Fig. 2.16 ). During athero-
sclerosis, monocyte adherence to the endothelium is one of the earliest steps in
lesion development. A monocyte entering the arterial wall at a junction between the
endothelial cells consume excess Low Density Lipoprotein (LDL) that is present
in the arterial wall, and then transform into macrophages. The macrophages then
consume more LDL and then oxidize to become foam cells. The accumulation of
foam cells can damage the arterial wall increasing its permeability and the rate of
plaque build-up. When the plaque ruptures and a thrombus blocks the blood flow
path, the tissue suffers from a lack of oxygen supply, which results in myocardial
ischemia and lead to myocardial infarction (heart attack) or angina pectoris (chest
pain from an ischemia).
Fig. 2.16  Narrowing of lumen based on build-up of plaque over time. The localization of plaque
and its growth takes place over time and results in lumen narrowing. This further aggravates the
growth of plaque. When plaque ruptures, the platelets of the blood tend to adhere to the cytokines
at the arterial wall at the injury site to form a clot that blocks the flow completely. Eventually, a
complete blockage results to obstruct the entire blood supply
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