Atherosclerosis is a form of arteriosclerosis. Atherosclerosis is the hardening of the arteries caused by cholesterol plaque deposits. It can occur in the coronary arteries, the carotid arteries, the aorta, and the leg arteries. Healthy arteries are flexible, strong, and elastic. The inner layer, the tunica interna, is smooth, enabling blood to flow freely. As a person ages, the arteries normally become thicker and less elastic, and their calcium content increases. This natural ' hardening' process occurs throughout the artery system.
Atherosclerosis, by contrast, affects only the larger arteries. As the plaque builds up, the inner layers of the artery walls become thick and irregular. Fat, cholesterol, and other materials accumulate in certain areas. This gradual build-up over a long period of time reduced the circulation of blood and increases the risk of heartattack, stroke, and other serious arterial diseases. A person having atherosclerosis will often experience symptoms of angina, stroke, and claudication. All of the symptoms are caused by insufficient blood flow due to atherosclerosis. Initially, the deposits of fat-containing cells that lead to atherosclerosis are only slight streaks, and are called fatty streaks. As the fatty streaks enlarge, they invade the deeper layers of the artery walls, causing scarring and calcium deposits. Large deposits are called athermas or plaques. The plaques calcify into a chalky substance. The plaque consists of a firm shell that contains calcium with areas of fatty material, and a centre consisting of soft cholesterol. As the plaque deposits grow the cardiac muscle beyond the blockage becomes deprived of blood, a condition known as myocardial ischemia. The healthy elastic wall of the artery changes into dead and unresponsive scartissue. If insufficient blood flow continues, the cardiac muscle dies, causing myocardial infarction. As the degeneration of the endothelial lining of the arteries continues, the lining may be damaged. Bloodplatelets stick to the site of injury, and a chemical signal is activated that promotes an influx of cholesterol.
The symptoms of atherosclerosis develop slowly as the development of the occlusion of the arteries progresses. Symptoms include angina, stroke, and claudication. The specific symptoms depend on which artery or arteries are occluded. If the leg arteries are affected, symptoms usually include numbness, fatigue, or pain in the leg. Occlusion of the coronary arteries may lead to angina or even a heartattack. When atherosclerosis occurs in the coronary arteries, it can lead to myocardial ischemia, an insufficient flow of blood to the heart. If the duration of ischemia is brief, the damage is reversible. However, if the duration of ischemia is longer than 40 to 60 minutes, irreversible damage may occur, and the parts of the heart muscle deprived of blood become permanently damaged, leading to myocardial infarction. Other commonly affected large arteries include the carotid arteries and the abdominal aorta. Initially, the symptoms of atherosclerosis are more likely to occur during exercise or strenuous activity than at rest. The symptoms develop during exercise because the arteries cannot supply the muscles with enough oxygen and nutrients. This process results in the build-up of by-products in the muscle that cannot be removed efficiently because of the occluded blood flow. This build-up of waste products, such as lactic acid, causes pain. It is similar to the build-up of lactic acid in muscles due to overexertion. As the narrowing of the arteries increases, the symptoms become prevalent with less and less exertion. The symptoms generally disappear after a few minutes of rest. However, the occlusion can be so severe that even the resting muscle does not get enough blood flow and the symptoms may be experienced even when sitting still. Research Atherosclerosis
Blood is one of the three main fluids in the body (the other two are the fluid around cells and the fluid inside the cells). It supplies oxygen, transports nutrients, waste, and hormonal messengers to each of the sixty billion cells in the body, as well as defending the body against foreign material. There are close to 30 trillion blood cells in an adult. Each cubic millimeter of blood contains from 4 1/2 to 5 1/2 million red blood cells and an average total of 7,500 white blood cells.
Blood has four main components: red blood cells, white blood cells, platelets, and liquid plasma. Since both red and white blood cells are continually being destroyed, the body must continue to produce new ones. About 2 1/2 million red blood cells die every second, at the same time, about 2 1/ 2 million new ones are created. Research Blood
Haemostasis is natural or surgical stoppage of bleeding. In the natural mechanism, the damaged vessel contracts, restricting the flow, and bloodplatelets plug the opening, releasing chemicals essential to clotting. Research Haemostasis
The kidneys are two, bean-shaped organs are located in the posterior of the abdomen. They generally are not thought of as endocrine organs.
The major function of the kidneys is the filtering toxins, wastes, ingested water, and mineral salts out of the bloodstream. However, the kidneys also serve a number of important endocrine functions.
They produce a substance called renin, which is an important enzyme in controlling blood pressure. When blood pressure falls, the kidneys release renin, which converts angiotensisnogen to the protein angiotensin I. This protein is then converted to angiotensin II,a protein which constricts blood vessels and thereby increases blood pressure. Angiotensis II also stimulates the release of aldosterone, a hormone that increases blood pressure.
Platelets are tiny specialized cells that are activated whenever blood clotting or repair to a vessel is necessary. Although they are often called cells, they are really fragments of other cells. They are made in bonemarrow and are much smaller than red blood cells. A drop of blood contains some 15 million platelets. When a blood vessel is cut, platelets rush to the vessel and swell into odd, irregular shapes, grow sticky and clog at the cut, creating a plug. If the cut is too large for platelets, they send out signals to initiate clotting by releasing a hormone called serotonin, which stimulates blood vessels to contract thus reducing the flow of blood. Clotting is fundamentally a change of the soluble plasmaproteinfibrinogen into an insoluble, thread-like protein, called fibrin. More than a dozen factors are involved in this conversion. The fibrin strands mesh around the blood cells and then contract, squeezing a clear yellowish fluid called serum, and forming a solid clot. Clotting staunches bleeding and creates a scaffold on which to build new tissue. Research Platelets
Thrombocytopenic purpura is a bleeding condition in which there is a shortage of platelets due to excessive destruction. It is treated by removing the spleen (splenectomy). Occasionally blood transfusion is required at such an operation, but there is very little risk of bleeding being excessive since the number of platelets in the blood rises rapidly once the spleen, which has been destroying them, is removed. In fact, the number of platelets circulating in the blood for the few days following the operation may become so excessive that spontaneous thrombosis may occur in veins. Research Thrombocytopenic Purpura
The Probert Encyclopaedia was designed, edited and programed by
Matt and Leela Probert
Abbreviations
Research Atherosclerosis
