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MODULE CODE: BPT1501
MAY JUNE PORTFOLIO 2023
DECLARATION
HAVING READ UNISA'S POLICY TOWARDS PLAGIARISM, I DO HEREBY DECLARE THAT THIS IS MY OWN WORK AND I HAVE NOT SHARED WITH ANYONE ELSE, WHERE I HAVE USED EXTERNAL SOURCES, I ...
Question 1
Atherosclerosis thickening or hardening of the arteries. It is caused by a buildup of
plaque in the inner lining of an artery.
Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products,
calcium, and fibrin. As it builds up in the arteries, the artery walls become thickened and
stiff.
Atherosclerosis is a leading cause of mortality and morbidity in the western world. It has
been recognized for over a century, and the understanding of its pathogenesis has
undergone many changes. Pathophysiological studies have unravelled the interactions
of molecular and cellular elements involved in atherogenesis. The focus has shifted to
the novel risk factors as well as characteristics and stability of atherosclerotic plaque;
the genetic predisposition has further broadened the pathogenetic mechanisms.
This review focuses on the molecular mechanisms involved in the evolution of the
atherosclerotic plaque that may pave the way for selecting optimal therapies and
preventing plaque complications. Atherosclerosis is no longer a disease attributed
mainly to the high lipid content of the body. New insight into the disease pathology has
shown it to be a disease of much greater ramifications. Endothelial damage and
reactive oxygen species (and other free radicals) have predominantly emerged as
factors in virtually all pathways leading to the development of atherosclerosis due to
hyperlipidemia, diabetes, hypertension or smoking. Novel risk factors such as
hyperhomocysteinemia, infections and systemic lupus erythematosus have emerged.
Atherosclerosis has come to be regarded as a chronic inflammatory disease with an
autoimmune component. The genetic basis of the disease assumes significance as
candidate genes are identified and gene therapy becomes a promising new addition to
the existing, less substantial conventional therapies.
Atherosclerosis is a slow, progressive disease that may start as early as childhood.
However, it can progress rapidly.Signs and symptoms of atherosclerosis may develop
gradually, and may be few, as the plaque gradually builds up in the artery. Symptoms
may also vary depending on the affected artery. However, when a major artery is
blocked, signs and symptoms may be severe, such as those occurring with heart attack,
stroke, or blood clot.
The symptoms of atherosclerosis may look like other heart conditions. See your
healthcare provider for a diagnosis. The procedure, a long thin tube (catheter) is passed
into the coronary arteries. X-rays are taken after a dye is injected into an artery to locate
the narrowing, blockages, and other abnormalities of specific arteries.
, Doppler sonography. A special probe is used to direct sound waves into a blood vessel
to evaluate blood flow. An audio receiver amplifies the sound of the blood moving
though the vessel. Faintness or absence of sound may mean there is a blockage. This
is used to identify narrowing of the blood vessels of the abdomen, neck, or legs.
Blood pressure comparison. Comparing blood pressure measurements in the ankles
and in the arms helps determine any constriction in blood flow. Significant differences
may mean blood vessels are narrowed due to atherosclerosis.
MUGA/radionuclide angiography. This is a nuclear scan to see how the heart wall
moves and how much blood is expelled with each heartbeat, while the person is at rest.
Thallium/myocardial perfusion scan. This is a nuclear scan given while the person is at
rest or after exercise that may reveal areas of the heart muscle that are not getting
enough blood.
Atherosclerosis starts early in life, and some studies have shown that maternal
hypercholesterolemia during pregnancy is associated with a marked increase in the
formation of fatty streaks in the human fetus . The disease appears earliest in the aorta
(during fetal life), while it appears in the coronary arteries in the second decade and in
the cerebral arteries in the third decade. Some lesions regress while others become
complicated. Focal development of the lesions is seen at predisposed sites such as the
branch points, whereas the proximal parts and the curvatures of smaller vessels have a
higher predilection.
Question 2
Disseminated intravascular coagulation (DIC) is a rare but serious condition that causes
abnormal blood clotting throughout the body’s blood vessels. You may develop DIC if
you have an infection or injury that affects the body’s normal blood clotting process.DIC
progresses through two stages: overactive clotting followed by bleeding.
In stage one, overactive clotting leads to blood clots throughout the blood vessels. The
clots can reduce or block blood flow, which can damage organs.
In stage two, as DIC progresses, the overactive clotting uses up platelets and clotting
factors that help the blood to clot. Without these platelets and clotting factors, DIC leads
to bleeding just beneath the skin, in the nose or mouth, or deep inside the body.
Disseminated intravascular coagulation (DIC) is defined by the International Society of
Thrombosis and Haemostasis (ISTH) as an acquired syndrome characterized by the
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