Pharmacy Clinic
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Cholesterol and Hypercholesterolemia
CHOLESTEROL
Cholesterol is an important component of cell membranes and is vital to the
structure and function of all cells in your body. However, cholesterol is a
pre-dominant substance in antherosclerotic plaque, which may develop in arteries and
impede the flow of blood. Cholesterol is not the only lipid circulating in your blood
stream. Triglycerides are another form of fat that circulates in the blood. Cholesterol
and Triglycerides being fats cannot dissolve in water. Therefore, to circulate through
your blood which is mainly water they must be carried by protein packages called
Apoproteins. The combination of Apoprotein and Lipid is known as lipoproteins.
The main type of Lipoproteins are Low Density Lipoproteins (LDL a combination of
25% Apoproteins and 45% Cholesterol. It provides cholesterol for necessary body
functions but in excessive amounts, it promotes cholesterol accumulation in the
artery walls. High-density cholesterol is a combination of 50% Apoprotein and 20%
cholesterol. HDL tends to help remove excess cholesterol from your blood. Therefore,
a relatively low ratio of LDL to HDL is desirable for lowering your risk for development
of coronary artery disease.
Lipid levels and
Coronory Risk Desirable Borderline High Risk
Total cholesterol < 200 200-233 > 240
LDL < 130 130-159 >160
Triglycerides < 200 200-500 > 500
HDL > 45 35-45 < 35
How to calculate your LDL Cholesterol Level.
Total Cholesterol - HDL - 1/5 Triglycerides = LDL
Many times the blockages are incomplete and develop over time gradually narrowing
the artery until the blood flow is nearly stopped. In some cases the body can
compensate for these narrowing by developing small branches call Collateral's that
bypass the narrowed sectors in blockages. The Collateral's are helpful but are not
always enough to restore circulation. We need cholesterol for a number of body
functions to manufacture adrenal and sex harmones to produce bile acids used in
digestion to build cell walls and to form protective sheath around nerves. Because
cholesterol is so important, the body makes its own supply from the liver.
Very Low Density Lipoproteins is a substance that the liver uses to manufacture LDL.
Scientists refer VLDL as a precursor of LDL. The higher the VLDL the more LDL can be
produced by the liver. Triglycerides are also harmful because it is the major
component of VLDL, which in turn leads to increased LDL in the blood.
High levels of cholesterol in the blood and Heart diseases
A common explanation is the injury theory. The disease begins when the thin
protective layer of cells endothelium that lines the arteries become damaged. This
damage can result from high blood pressure which forces the blood against the artery
walls with extraordinary power, excessive smoking and cholesterol.
Normally injury to a healthy artery lining is swiftly repaired but not after the onset of
atherosclerosis. Too much cholesterol, high blood pressure or smoking hinders the
normal healthy process. On any damage, first to arrive may be small blood cells
called platelets, normally associated with clotting. The Platelets emit chemical signals
that cause smooth cells - Usually confined between endothelium and the other layer
of the artery - to find their way to the damaged area. There they may multiply
Quickly to produce a mesh of elastic fibers and connective tissues
The injured cell interrupts blood flow, which causes cells to be torn from the watery
walls causing exposure. Once these epithelial cells are injured, they are unable to
protect arterial walls. Monocyte a special type of blood cell attaches to the injured
cells as an effort to heal them. At the same time, platelets a type of blood cell that
helps stop bleeding begin to adhere to the underlying elastic cells. The chemical
reaction of the platelets, endothelial cells and monocyte create a substance that
causes the smooth muscle cell in the middle layer replicate more rapidly forming an
unnatural dome. The dome of smooth muscle eventually protrudes into the central
core of the artery diminishing the flow of blood. The development of smooth muscle
cell thickening in the arterial walls is the first pathological step in the process of
atherosclerosis. Once the endothelium is broken, molecules of fat actually stick to the
smooth muscle cells that have formed the domes. Therefore the dome balloon outs
and projects farther and farther into the artery. As plaque enlarges they accumulate
more and more muscle cells elastic fibers and lipid fat deposits. Within the center of
the plaques calcium crystals begin to form. They project so far into the arteries that
they actually block blood flow enough to produce angina or chest pain. The plaque
can rupture at any time and if so releases the dead cells, crystals and fat molecule
into the blood stream. It can create a blood clot and block an artery or attract
platelets. Blood platelets stick to the site of the injury and a chemical signal is
activated that promotes an influx of cholesterol. Cholesterol and other substances
such as calcium build up in the artery walls. Eventually plaque forms that bulges into
the blood stream and impedes blood flow through the artery.
Macrophages large white cells in the vessel wall that become free during injury
contribute to the chaos by rushing in and filling up with cholesterol from blood. The
conglomeration of cells become engorged bursts and releases its cholesterol. More
white cells arrive to clean up the debris . These in turn become distended and
explode. The accumulating mass forms a patch called Plaque, which may seriously
obstruct the flow of blood, This damage can lead to heart attack, a stroke or chest
pain.
Cholesterol is an important component of cell membranes and is vital to the
structure and function of all cells in your body. However, cholesterol is a
pre-dominant substance in antherosclerotic plaque, which may develop in arteries and
impede the flow of blood. Cholesterol is not the only lipid circulating in your blood
stream. Triglycerides are another form of fat that circulates in the blood. Cholesterol
and Triglycerides being fats cannot dissolve in water. Therefore, to circulate through
your blood which is mainly water they must be carried by protein packages called
Apoproteins. The combination of Apoprotein and Lipid is known as lipoproteins.
The main type of Lipoproteins are Low Density Lipoproteins (LDL a combination of
25% Apoproteins and 45% Cholesterol. It provides cholesterol for necessary body
functions but in excessive amounts, it promotes cholesterol accumulation in the
artery walls. High-density cholesterol is a combination of 50% Apoprotein and 20%
cholesterol. HDL tends to help remove excess cholesterol from your blood. Therefore,
a relatively low ratio of LDL to HDL is desirable for lowering your risk for development
of coronary artery disease.
Lipid levels and
Coronory Risk Desirable Borderline High Risk
Total cholesterol < 200 200-233 > 240
LDL < 130 130-159 >160
Triglycerides < 200 200-500 > 500
HDL > 45 35-45 < 35
How to calculate your LDL Cholesterol Level.
Total Cholesterol - HDL - 1/5 Triglycerides = LDL
Many times the blockages are incomplete and develop over time gradually narrowing
the artery until the blood flow is nearly stopped. In some cases the body can
compensate for these narrowing by developing small branches call Collateral's that
bypass the narrowed sectors in blockages. The Collateral's are helpful but are not
always enough to restore circulation. We need cholesterol for a number of body
functions to manufacture adrenal and sex harmones to produce bile acids used in
digestion to build cell walls and to form protective sheath around nerves. Because
cholesterol is so important, the body makes its own supply from the liver.
Very Low Density Lipoproteins is a substance that the liver uses to manufacture LDL.
Scientists refer VLDL as a precursor of LDL. The higher the VLDL the more LDL can be
produced by the liver. Triglycerides are also harmful because it is the major
component of VLDL, which in turn leads to increased LDL in the blood.
High levels of cholesterol in the blood and Heart diseases
A common explanation is the injury theory. The disease begins when the thin
protective layer of cells endothelium that lines the arteries become damaged. This
damage can result from high blood pressure which forces the blood against the artery
walls with extraordinary power, excessive smoking and cholesterol.
Normally injury to a healthy artery lining is swiftly repaired but not after the onset of
atherosclerosis. Too much cholesterol, high blood pressure or smoking hinders the
normal healthy process. On any damage, first to arrive may be small blood cells
called platelets, normally associated with clotting. The Platelets emit chemical signals
that cause smooth cells - Usually confined between endothelium and the other layer
of the artery - to find their way to the damaged area. There they may multiply
Quickly to produce a mesh of elastic fibers and connective tissues
The injured cell interrupts blood flow, which causes cells to be torn from the watery
walls causing exposure. Once these epithelial cells are injured, they are unable to
protect arterial walls. Monocyte a special type of blood cell attaches to the injured
cells as an effort to heal them. At the same time, platelets a type of blood cell that
helps stop bleeding begin to adhere to the underlying elastic cells. The chemical
reaction of the platelets, endothelial cells and monocyte create a substance that
causes the smooth muscle cell in the middle layer replicate more rapidly forming an
unnatural dome. The dome of smooth muscle eventually protrudes into the central
core of the artery diminishing the flow of blood. The development of smooth muscle
cell thickening in the arterial walls is the first pathological step in the process of
atherosclerosis. Once the endothelium is broken, molecules of fat actually stick to the
smooth muscle cells that have formed the domes. Therefore the dome balloon outs
and projects farther and farther into the artery. As plaque enlarges they accumulate
more and more muscle cells elastic fibers and lipid fat deposits. Within the center of
the plaques calcium crystals begin to form. They project so far into the arteries that
they actually block blood flow enough to produce angina or chest pain. The plaque
can rupture at any time and if so releases the dead cells, crystals and fat molecule
into the blood stream. It can create a blood clot and block an artery or attract
platelets. Blood platelets stick to the site of the injury and a chemical signal is
activated that promotes an influx of cholesterol. Cholesterol and other substances
such as calcium build up in the artery walls. Eventually plaque forms that bulges into
the blood stream and impedes blood flow through the artery.
Macrophages large white cells in the vessel wall that become free during injury
contribute to the chaos by rushing in and filling up with cholesterol from blood. The
conglomeration of cells become engorged bursts and releases its cholesterol. More
white cells arrive to clean up the debris . These in turn become distended and
explode. The accumulating mass forms a patch called Plaque, which may seriously
obstruct the flow of blood, This damage can lead to heart attack, a stroke or chest
pain.
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