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الكلية كلية طب الاسنان
القسم العلوم الاساسية
المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي
5/31/2011 7:59:00 AM
Vascular diseases:
Introduction : The role of arterial system is to distribute blood from the heart throughout the body.
types of vessels in arterial system are:
1- Elastic arteries (aorta, subclavian, carotid,..)
2- muscular arteries (coronary, radial, femoral,..)
3- arterioles (terminal branches). Histology: the arteries in general composed from the following layers: Tunica intima: Single layer of flattened endothelial cells, supported by fibroblasts & smooth muscle cells. Tunica media: Sheets of elastin, collagenous tissue and smooth muscle cells fibers. Tunica adventitia: Collagenous supportive external layer.
Atherosclerosis
Arteriosclerosis literally means hardening of the arteries. clinical significance Atherosclerosis contributes to more mortality, "approximately half or more of all deaths", and serious morbidity in the Western world than any other disorder. Significant progress has been made over the last decades in the United States and elsewhere. there was an approximately 50% decrease in the death rate from ischemic heart disease and a 70% decrease in death from strokes, a reduction in mortality that has increased the average life expectancy in the United States by 5 years.
The basis for this trend has been attributed to
(1) prevention of atherosclerosis through changes in living habits, including reduced cigarette smoking, altered dietary habits with reduced consumption of cholesterol and other saturated animal fats, and control of hypertension
(2) improved methods of treatment of myocardial infarction and other complications of ischemic heart disease. Atherosclerosis primarily affects elastic arteries (aorta, carotid and iliac arteries) and large and medium-sized muscular arteries (coronary and popliteal arteries).
The disease often begins in childhood, but symptoms are not usually evident until middle age or later when the arterial lesions precipitate organ injury Although any organ or tissue in the body may be so involved, symptomatic atherosclerotic disease is most often localized to the arteries supplying the heart, brain, kidneys, lower extremities, and small intestine. Myocardial infarction (heart attack), cerebral infarction (stroke), and aortic aneurysms are the major consequences of this disease. Atherosclerosis also takes a role in chronically diminished arterial perfusion, such as gangrene of the legs, chronic ischemic heart disease, and ischemic encephalopathy.
EPIDEMIOLOGY : Atherosclerosis is virtually common among the populations of North America, Europe, Australia, New Zealand, and other developed nations, it is much less prevalent in Central and South America, Africa, and Asia.
The risk factors:
Age. The disease is a slowly progressive disease that begins in childhood and develops slowly over decades. Death rates from ischemic heart disease rise with each decade even into advanced age. For example, from age 40 to age 60, there is a greater than fivefold increase in the incidence of myocardial infarction.
Sex. Men are much more prone to atherosclerosis and its consequences than women. Myocardial infarction and other complications of atherosclerosis are uncommon in pre menopausal women unless they are predisposed by diabetes or some form of hyperlipidemia or severe hypertension. After menopause, the incidence of atherosclerosis-related diseases increases, The frequency of myocardial infarction becomes the same in both sexes by the sixties to seventies.
Genetics. The well-established familial predisposition to atherosclerosis and ischemic heart disease is most likely polygenic. In some instances, it relates to familial clustering of other risk factors, such as hypertension or diabetes, whereas in others it involves well-defined hereditary genetic derangements in lipoprotein metabolism that result in excessively high blood lipid levels, such as familial hypercholesterolemia. The four major well-accepted modifiable conditions are hyperlipidemia, hypertension, cigarette smoking, and diabetes.
Hyperlipidemia. Hyperlipidemia is acknowledged to be a major risk factor for atherosclerosis. Most of the evidence specifically implicates hypercholesterolemia; hypertriglyceridemia plays a less significant role, but its effect may be greater in women than men. The major component of the total serum cholesterol that is associated with increased risk is low-density lipoprotein (LDL) cholesterol. In contrast, there is an inverse relationship between symptomatic atherosclerosis and high-density lipoprotein (HDL) level; thus, the higher the levels of HDL, the lower is the risk of ischemic heart disease. Other genetic or acquired disorders (e.g., diabetes mellitus, hypothyroidism) that cause hypercholesterolemia lead to premature and severe atherosclerosis. The major lipids in atheromas (plaques) are cholesterol and cholesterol esters derived from the plasma. When levels of serum cholesterol are lowered by diet or drugs, the rate of progression of atherosclerotic disease is slowed, some atherosclerotic plaques regress, and the risk of cardiovascular events is reduced. Cholesterol lowering increases overall survival and reduces risk of atherosclerosis-related events in patients with established coronary heart disease with elevated or average cholesterol levels as well as in patients with hypercholesterolemia but without overt atherosclerosis-related disease. High dietary intake of cholesterol and saturated fats, such as those present in egg yolk, animal fats, and butter, raises the plasma cholesterol level. Conversely a diet low in cholesterol and low in the ratio of saturated to polyunsaturated fats lowers plasma cholesterol levels.
Hypertension. Hypertension is a major risk factor for atherosclerosis at all ages. Men at age 45 to 62 whose blood pressure exceeds 169/95 mm Hg have a more than fivefold greater risk of ischemic heart disease than those with blood pressures of 140/90 mm Hg or lower. Both systolic and diastolic levels are important in increasing risk. Antihypertensive therapy reduces the incidence of atherosclerosis-related diseases, particularly strokes and ischemic heart disease.
Cigarette Smoking. Cigarette smoking is not only a well-established risk factor in men, but also is thought to account for the relatively recent increase in the incidence and severity of atherosclerosis in women. When one or more packs of cigarettes are smoked per day for several years, the death rate from ischemic heart disease increases by up to 200%.
Diabetes Mellitus. Diabetes mellitus induces hypercholesterolemia and a markedly increased predisposition to atherosclerosis. Other factors being equal, the incidence of myocardial infarction is twice as high in diabetics as in non diabetics. There is also an increased risk of strokes and, even more striking, perhaps a 100-fold increased risk of atherosclerosis-induced gangrene of the lower extremities. In the absence of diabetes, atherosclerotic gangrene of the lower extremities is uncommon. Elevated Plasma Homocysteine. Homocystinuria refers to a group of rare inborn errors of metabolism resulting in high levels of circulating homocysteine. Patients with this condition have premature vascular disease. There is evidence that homocysteine may cause endothelial dysfunction, through formation of reactive oxygen species that play an important role in atherogenesis. It also interferes with the vasodilator function of nitric oxide. Factors Affecting Hemostasis and Thrombosis. Epidemiologic evidence also indicates that several markers of hemostatic and thrombotic function, in addition to homocysteine level, are potent predictors of risk for major atherosclerotic events, including myocardial infarction and stroke. Reduction of incidence of first myocardial infarction associated with the use of aspirin.
Other Factors. Other factors associated with a less pronounced or difficult-to-quantitate risk include lack of exercise, competitive, stressful life style with type A personality behavior, and unrestrained weight gain (largely because obesity induces hypertension, diabetes, hypertriglyceridemia, and decreased HDL
Morphology:
Fatty Streak. They may be precursors of the atheromatous plaques. The streaks begin as multiple yellow; flat spots (fatty dots) less than 1 mm in diameter that coalesce into elongated streaks; 1 cm long or longer. Fatty streaks are composed of lipid-filled foam cells with T lymphocytes and extra cellular lipid present in smaller amounts than in plaques. Fatty streaks appear in the aortas of some children younger than 1 year of age and all children older than 10 years, regardless of geography, race, sex, or environment. Coronary fatty streaks are less common than aortic but begin to form in adolescence, and they occur at the same anatomic sites that are later prone to develop plaques.
Atheromatous Plaque. The basic lesion consists of a raised focal plaque within the intima, having a core of lipid (mainly cholesterol and cholesterol esters) and a covering fibrous cap. They also called fibro fatty plaques. atheromatous plaques appear white to whitish yellow in color. They vary in size from approximately 0.3 to 1.5 cm in diameter but sometimes coalesce to form larger masses.
On section, the superficial portion of these lesions at the luminal surface tends to be firm and white (the fibrous cap) and the deep portions yellow or whitish yellow and soft. Atherosclerotic plaques have three principal components:
(1) cells, including smooth muscle cells, macrophages, and other leukocytes.
(2) connective tissue extra cellular matrix, including collagen, elastic fibers, and proteoglycans.
(3) intracellular and extra cellular lipid deposits. These three components occur in varying proportions in different plaques, giving rise to a spectrum of lesions. Typically the superficial fibrous cap is composed of smooth muscle cells with a few leukocytes and relatively dense connective tissue; a cellular area beneath and to the side of the cap (the shoulder), consisting of a mixture of macrophages, smooth muscle cells, and T lymphocytes; and a deeper necrotic core, in which there is a disorganized mass of lipid material, cholesterol clefts, cellular debris, lipid-laden foam cells, fibrin, thrombus in various stages of organization, and other plasma proteins.
The complicated lesion of atherosclerosis, defined by the following changes, has the most clinical significance:
1-Patchy or massive calcification. Arteries may become virtual pipe stems, and the aorta may assume an eggshell brittleness. Patients with high coronary artery calcium appear to be at increased risk for coronary events. Using calcification as a marker, new technologies such as computed tomography and intravascular ultrasound may provide an accurate noninvasive approach to diagnosis.
2-Focal rupture or gross ulceration of the luminal surface of atheromatous plaques may result in exposure of highly thrombogenic substances that induce thrombus formation or discharge of debris into the bloodstream, producing micro-emboli (cholesterol emboli or atheroemboli).
3-Hemorrhage into a plaque may occur, especially in the coronary arteries, Thrombi may partially or completely occlude the lumen; they may become incorporated within the intimal plaque by organization.
4- Although atherosclerosis is initially an intimal disease, in severe cases, particularly in large vessels, the underlying media undergoes considerable atrophy with loss of elastic tissue (causing sufficient weakness to permit aneurismal dilation).
pathogenesis two hypotheses for atherogenesis: One emphasized cellular proliferation in the intima as a reaction to plasma proteins and lipids from the blood. Second one postulated that organization and repetitive growth of thrombi resulted in plaque formation. The new hypothesis called the response to injury hypothesis, considers atherosclerosis to be a chronic inflammatory response of the arterial wall initiated by some form of injury to the endothelium. Central to this thesis are the following events: 1- focal regions of chronic endothelial injury lead to endothelial dysfunction.
2- increased endothelial permeability and increased leukocyte adhesion.
3-migration of monocytes into the intima and their transformation into macrophages and foam cells .
4- Adhesion of platelets to focal areas.
5-migration of smooth muscle cells from media into the intima.
6-Enhanced accumulation of lipids both within cells (macrophages and smooth muscle cells) and extracellularly .
Recent hypothesis: There is current interest in whether infectious processes could contribute to atherosclerosis Viruses can cause vasculitis and both herpes virus and cytomegalovirus have been detected in human atheromatous plaques, and recently Chlamydia pneumoniae has been demonstrated in atherosclerotic plaques b
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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