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  2. Arteriosclerosis .. is a general term for several diseases where the arterial walls become thick and lose elasticity independently of cause this thickening. There are five main form of arteriosclerosis: 1. atherosclerosis (the most common). 2. Mönckeberg’s arteriosclerosis (calcification of small arteries, usually in the elderly, also called medial calcific sclerosis). 3. Inflammatory arteriosclerosis (syphilitic). 4. Hyperplastic arteriolosclerosis is associated with malignant hypertension or necrotizing vasculitis and is characterized by "onionskin hyperplasia," i.e., concentric thickening of the intima, deposition of basophilic ground substance, smooth muscle proliferation, and hypertrophy of the adventitia. 5. Hyaline arteriolosclerosis is associated with diabetes, hypertension, and old age. Arteriolar sclerosis (arteriolosclerosis, mostly caused by hypertension in arterioles particularly in the kidney, spleen and pancreas).It is characterized by hyaline thickening of arterioles that narrows the vessel lumen.
  3. Atheroscleros is is a type of arteriosclerosis. It comes from the Greek words athero (meaning gruel or paste) and sclerosis (hardness). Atherosclerosis is a chronic disease affecting primarily the intima of large and medium- sized arteries and is characterized by fibrolipid plaques or atheromas. Atherosclerosis is the commonest arterial diseases. Epidemiology. It is known that the most common cause of death (40%) is cardiovascular diseases, most of witch are related to atherosclerosis. Epidemiologic investigations on living populations have revealed a number of risk factors, which are associated with increased risk of developing clinical atherosclerosis. The risk factors are often acting in combination rather than singly. The first of them is age. Early atherosclerotic lesions may be present in childhood, but clinical manifestations will appear later. In scientific research, which have been performed at our department, morphological signs of atherosclerosis were found in the fetus and new- born aorta. The second of risk factors is sex. The incidence and severity of atherosclerosis are higher in men than in women. Genetic factors play a significant role in atherosclerosis. There is familial predisposition to atherosclerosis which may be related to other risk factors like diabetes, hypertension and hyperlipoproteinemia. Geographic factors also play a role. There is a high incidence of atherosclerosis in the Europe, Australia, and US.
  4. Hyperlipidemia. Elevated serum cholesterol levels, especially low density lipoprotein (LDL) and very low-density lipoprotein (VLDL). Many studies have demonstrated specific effects of diet including the amount of dietary cholesterol ingested on lipid and lipoprotein levels. Hypertension is a major risk factor in atherosclerosis development. It acts probably by mechanical injury to the arterial wall due to increased blood pressure. Other factors are diabetes mellitus, smoking, obesity, etc.
  5. Pathogenesis There are several pathogenesis theories of atherosclerosis: Virchow's, Rokitansky's, Anychkow's, Benditt's. Historically, two hypotheses for atherogenesis were dominant: one emphasized cellular proliferation in the intima as a reaction to insudation of plasma proteins and lipids from the blood, whereas the other postulated that organization and repetitive growth of thrombi resulted in plaque formation. The contemporary view of the pathogenesis of atherosclerosis incorporates elements of both older theories and is called the response to injury hypothesis. Formulated in 1973 and modified in 1986 and 1993, it states that atherosclerotic lesions are initiated as a response to some form of injury to arterial endothelium. The injury is a form of endothelia dysfunction without necessary denudation, which increases permeability to plasma constituents, including lipids, and permits blood monocytes and eventually platelets to adhere to endothelium. Monocytes adhere and subsequently enter the intima, transform into macrophages, and accumulate lipid to become foam cells, contributing, to the evolution of the lesion. Factors released from, activated platelets at the surface or monocytes then cause migration of smooth muscle cells from media into the intima followed by proliferation and synthesis of extracellular matrix components by smooth muscle.cells, leading to the accumulation of collagen and proteoglycans. Single or short-lived injurious events can be followed by restoration of endothelial function and regression of the lesion. Repeated or chronic injury, however, results in the development of an atheromatous plaque, probably by permitting continuing increased permeability, ingress of monocytes, or perhaps platelet interactions. One of the more recent theories suggests that excess lipoproteins, LDL, in the blood are trapped within the artery wall. When this happens and they accumulate, they become oxidized. That leads to "modified" lipoproteins which are rapidly taken up by smooth muscle cells. This, in turn, leads to the formation of foam cells that lead to the deposition of connective tissue cells and elements. Dislipoproteinemia – disturbance of ratio between low density lipoprotein (LDL), very low-density lipoprotein (VLDL) and high density lipoprotein (HDH) it is one of the main causes of atherosclerosis.
  6. Morphology . Although the fibrous and complicated plaques are the atherosclerotic lesions associated with disturbances in blood front that cause clinical disease states, the morphologic changes of diffuse intimal thickening and fatty streaks may be either precursors of the basic atherosclerotic lesion or stages in its development
  7. 1.Intimal thickening. Fibromuscular thickening of the intima of arteries may be a part of atherosclerotic process, particularly rapid during the first two decades of life. Macroscopically, the lesions may appear as small white areas of intimal cushion at the bifurcation and branching of arteries, or many be appear as «diffuse intimal thickening». Microscopically, the lesions consist of smooth muscle cells, fibrous tissue, some collagen but no lipid. 2.Fatty streaks especially prominent in the aorta and major arteries, more often on the posterior wall than the anterior wall. Macroscopically, the lesions may appear as flat or slightly elevated and yellow. They may be either in the form of small (about l mm in size) or in the form of elongated, beaded streaks. Microscopically, fatty streaks lying under the endothelium are composed of closely-packed foam cells, lipidcontaining elongated smooth muscle cells and a few lymphoid cells. Small amount of extracellular lipid, collagen and proteoglycans are also present. The cholesterol esters in foam cells of fatty streaks differ chemically from those in the lipid core of atheromatous fibrous plague. These dissimilarities might be explained on the basis of two types of fatty streaks, which differ in morphology, cellular genotype, and lipid content, with one type related to the fibrous plague and the other type not related 3. Fibrous plaque (atheroma). The lesions are raised, pearly white to grey, smooth-surfaced, plaque like structures in the intima but may extend into the media, may encroach considerably on the vascular lumen, especially in muscular arteries such as coronary arteries. On cross section a typical lesion has a soft, yellow central zone with gruel-like material covered on the luminal aspect by a layer of dense fibromuscular tissue (fibrous cap). In general, plaques are found most often in the abdominal aorta, large arteries of the lower limbs, carotid arteries, proximal portions of the coronary arteries and circle of Willis. The histologic appearance of lesions varies considerably depending on the relative amounts of the different components. The central atheroma of an uncomplicated fibrous plague consist of acellular, amorphous, electron-dense material that contains lipids, cellular debris, fibrin and other plasma proteins. The fibrous cap is composed of avascular connective tissues and elongated smooth muscle cells covered by endothelium. Inflammatory cells, including macro-phages, may be present. In older and more advanced lesions the collagen in the fibrous cap may be dense and hyalinised, smooth muscle cells may be atrophic and foam cells are fewer.
  8. 4. Complicated plaques develop from preexisting fibrous plaques as a result of one of a combination of several pathologic changes that include calcification, ulceration, thrombosis and haemorrhage. The complicated lesion is the most common type of atherosclerotic lesion that produces significant circulatory change and clinical disease. A..Calcification the intima is brittle and cracks like an eggshell when the vessel is opened. Micro scopically the dystrophic calcific process involves both the fibrous cap and the atheromatous portion of the plaque. B..Ulceration and thrombosis. Advanced fibrous plaques with soft pultaceous atheromas, especially those with calcification may ulcerate as a result of mechanical or hemodynamic forces. With ulceration, cholesterol or lipid debris from the atheroma may be discharged and embolize. Mural thrombi may form on the ulcer or at sites of endothelial damage or mural hemorrhage. Such thrombi also may become organized and incorporated within the intimal plaque. Mural thrombi in medium-sized arteries may progress to occlusive thrombi that may reconalize. C..Hemorrhage into atherosclerotic plaque is a common finding in advanced lesions, especially in the coronary arteries. The blood may reach the lesion from the vascular lumen through surface ulcerations or from rapture of capillaries that vascularized the atheroma from adventitial vasa vasoram. D..With secondary changes in the media: 1) the internal elastic lamina is attenuated and fragmented. 2) smooth muscle cells and elastic lamina atrophy is connected a form of aneurysmal dilatation, which may follow, especially in elastic arteries.
  9. Microscopically following states of atherosclerosis are distinguished: 1. prelipidosis, 2. lipidosis, 3. liposclerosis, 4. atheromatosis, 5. ulceration, 6. atherocalcification.
  10. There are several clinico- morphological types of atherosclerosis according to localization. There are: 1) Atherosclerosis of aorta; 2) Atherosclerosis of coronary arteries; 3) Atherosclerosis of cerebral artery; 4) Atherosclerosis of arteries of lower extremities; 5) Atherosclerosis of arteries of small intestine; 6) Atherosclerosis of renal arteries.
  11. The clinical effects result from the following:  Slow luminal narrowing causing ischemia and atrophy.  Suddenly luminal occlusion causing infarction necrosis.  Propagation of plaque by formation of thrombi and emboli.  Formation of aneurysmal dilation and eventual rapture.
  12. The symptomatic atherosclerotic disease involves most often the heart, brain, kidneys, small intestine and lower extremities. Some of the important effects are listed below: Aorta aneurysm formation, thrombosis and embolization to other organs; Heart - myocardial infarction, ischemic heart disease; Brain - chronic ischemic brain damage (senile dementia), cerebral infarction; Small intestine - ischemic bowel disease, infarction; Lower extremities - intermittent claudication, gangrene. Kidney - chronic ischemic renal damage, sclerosis, atrophy. Aorta aneurysm is a wall bulge out. Aneurysms may be true and false. True aneurysms: all 3 tunics of the wall bulge out together False - Blood contained by a clot. Depend on the shape aneurysms may be fusiform, saccular. A dissecting aneurysm occurs when the layers of the artery separate from each other. Dissecting saccular aneurysm - blood is contained by the adventitia. This is a possible sequela of atherosclerosis. <6 cm rarely ruptures; 80% of larger ones rupture. Mortality: 5% pre-rupture 50% post-rupture. Most of them may be as a cause of death.
  13. ISCHAEMIC HEART DISEASE (CORONARY ARTERY DISEASE) Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. The World Health Organization’s Study group on Atherosclerosis and Ischemic Heart Disease defined ischemic heart disease (IHD) as the cardiac disability, acute and chronic, arising from reduction or arrest of blood supply to the myocardium in association with disease processes in the coronary arterial system. Synonymous: coronary heart disease (CHD), atherosclerotic heart disease (ASHD), coronary artery disease (CAD). The American Heart Association has classified risk factors developing IHD: Major risk factors cannot be changed: Heredity. Sex (gender).Race. Age. Major risk factors that can b changed: Cigarette smoking. Hypertension. Hypercholesterolemia. Diabetes mellitus. Contributing factors Obesity. Lack of physical exercise. Emotional stress Depending upon the suddenness of onset, duration, degree, location and extent of the area affected by myocardial ischemia, there can be 2 types of ischemic manifestation: acute and chronic.
  14. Acute: 1.Myocardial infarction. 2.Non-infarct effects of myocardial ischemia; which.include the following: A.angina pectoris; B.sudden cardiac death. Chronic: 1.Chronic atherosclerotic heart disease (atherosclerotic cardiosclerosis). 2.Postinfarction myocardiosclerosis. 3.Chronic aneurism of the heart.
  15. Myocardial infarction is the most significant in the human pathology. In industrialized countries myocardial infarction accounts for 10-25 % of all deaths. About 5 % of heart attacks occur in young people under the age of 40 years, especially with hypertension, diabetes mellitus, cigarette smoking and etc. Myocardial infarction is an ischemic myocardial cell necrosis. Etiology: causes of MI include coronary artery obstruction due to the progressive development of atherosclerosis; coronary artery spasm; embolism, thrombosis. Myocardial infarction has been classified in a number of ways by the physicians and the pathologists: 1.According to the anatomic region of the left ventricle involved. They are called anterior, posterior, lateral, septal and circumferential. 2.According to the degree of thickness of the ventricular wall involved: full-thickness or transmural, when they involve the entire thickness of the ventricular wall; subendocardial or lamina, when they occupy the inner subendocardial half of the myocardium, intramural, subepicardial. 3. According to the age of infarcts: A)newly-formed infarcts are called acute, recent or fresh; B)advanced infarcts are called old, healed or organized.
  16. Infarctions are most frequently located in the left ventricle. Beside it may be located in other parts of the heart. But it is observed rarely. The region of infarction depends upon the area of obstructed blood supply by one or more of the three coronary arterial trunks. 1.Stenosis of the left anterior descending coronary artery is the most common (40-50%). 2.Stenosis of the right coronary artery is the next most frequent (30-40%). 3. Stenosis of the left circumflex coronary artery is seen least frequently (15-20%). Pathologic changes. The macroscopic and microscopic changes in the myocardial infarction according to the age of the infarct. On gross examination, an acute myocardial infarct is not identifiable within the first 12 hours after the onset. By 24 hours, the infarct can be recognized on the cut surface of the involved ventricle by its pallor. After 3 to 5 days, the infarct is mottled and more sharply outlined, with a central pale, yellowish, necrotic region bordered by a hyperemic zone. By 2 to 3 weeks infracted region is depressed and soft, with a refractile, gelatinous appearance. Older, healed infarcts are firm and contracted and have the pale gray appearance of scar tissue. Microscopically the majority of infarcts occur singly and vary in size from 4 to 10 cm. During the first week the colour of infarct charges from cyanotic red to bright yellow or yellow-green. The consistency of infarct in this period is soft. During the second week infarct has red periphery and during the fourth to sixth week it is a thin, grey-white, hard, shrunken fibrous scar. Microscopically during the first week we may see coagulative necrosis and marginal neutrofilic infiltration, then beginning of resorption of necrosed fibres by macrophages, onset of fibrovascular response; neutrofilic infiltration disappear. During the fourth to sixth week-increased fibrocollagenic tissue, decreased blood supply, fewer pigmented macrophages, lymphocytes and plasma cells. Using special methods such as electron microscopy, chemical and histochemical studies, the changes can be demonstrated in early infarcts before detectable light microscopic alterations appear.
  17. Complications  About 10% patients with acute myocardial infarction develop cardiogenic shock, which is characterized by hypertension with systolic blood pressure of 80 mm Hg or less for many days.  Shock may be accompanied by peripheral circulatory failure, oliguria and mental confusion. A lot of patients with myocardial infarction suffer from congestive heart failure, which may be in the form of right ventricular, left ventricular failure or both. This complication is responsible for about 40% of deaths from acute myocardial infarction.  Arrhythmias are the most common form of complication in acute myocardial infarction.  Mural thrombosis and thromboembolism from intracardiac thrombi and from thrombosis in the leg veins is observed 15-45% in cases of acute myocardial infarction.  Usually in the first week heart rapture may develop. It is often fatal.  Cardiac aneurysm often develops in the left ventricle; it impairs the function of the heart and is a site for mural thrombi.  Fibrinous pericarditis appears on about the second day of myocardial infarction. As a rale, this complication develops in the patients with transmural myocardial infarction.  About 3-4% of patients who suffered from acute myocardial infarction develop post-myocardial infarction syndrome. It is characterized by pneumonitis. The main causes of death are complications of myocardial infarction.
  18. Non-infarct effects of myocardial ischemia 1.Angina pectoris is clinical syndrome of Coronary artery disease. Dystrophy and necrobiosis are revealed in the myocardial cells due to which transient myocardial pain in the substernal or pericardial region of the chest occurs. 2.Chronic Coronary artery disease (Myocardial fibrosis). Myocardial fibrosis may be focal or diffuse. Development mechanism of myocardial fibrosis can be different. Macroscopically the left ventricular wall generally shows the fact of grey-white fibrosis in brown myocardium. Microscopically there are areas of diffuse myocardial fibrosis, especially around the small blood vessels in the interstitial tissue of the myocardium. 3.Sudden cardiac death is defined as sudden death within 24 hours of the onset of cardiac symptoms. In the majority of cases it is caused by Coronary artery disease, coronary vasospasm, calcific aortic stenosis, myocarditis, hypertrophic cardiomyopathy, hereditary and acquired defects of the conduction system. The autopsy in such cases reveals most commonly critical atherosclerotic coronary narrowing.
  19. HYPERTANSIVE VASCULAR DISEASE In medically advanced countries, hypertension is the most common serious chronic disease, affecting about half the population over 50 years of age. Essential, primary, or idiopathic hypertension is defined as high blood pressure in which secondary causes such as renovascular disease, renal failure, pheochromocytoma, aldosteronism, or other causes of secondary hypertension or mendelian forms (monogenic) are not present. Essential hypertension accounts for 95% of all cases of hypertension. The World Health Organization has defined hypertension as a systolic pressure greater than 160 mm Hg or a diastolic pressure greater than 90 mm Hg, or both. Hypertensive heart disease or hypertensive cardiomyopathy is the disease of the heart resulting from systemic hypertension of prolonged duration and manifesting by left ventricular hypertrophy. Often hypertension predisposes to atherosclerosis. The arterial changes and vascular complications increase with the severity and duration of the hypertension, but are modified by genetic factors, environmental factors, sex (females tolerate hypertension better), and associated diseases. The increased peripheral resistance resulting in sustained hypertension may arise from: 1)increased sympathetic tone; 2) increased release of renin and generation of angiotensin (2); 3)the presence of vasoconstrictive substances in the circulation; 4)increased sodium load and extracellular fluid load and finally 5)a postulated excessive responsiveness to the other factors. In a given individual hypertension may be attributable to a combination of these factors.
  20. Hypertension is classified into two types 1.Primary or essential hypertension in which the cause of increase in blood pressure in unknown. This hypertension constitutes about 90—95% patients of hypertension. 2.Secondary hypertension, in which the increase in blood pressure is caused by diseases of the kidneys, endocrine or some other organs. This hypertension comprises 5-10% causes of disease. According to the clinical course, both types of hypertension may be benign or malignant. Benign hypertension is moderate elevation of blood pressure and the rise is slow as the years pass. About 90% patients of hypertension have benign disease. Malignant hypertension is marked and rapid increase of blood pressure to 200/140 mm Hg or more and the patients have papilledema, hemorrhages and hypertensive encephalopathy.
  21. Primary (essential) hypertension The cause of this hypertension is unknown. But there are a lot of factors are related to its development. There are as under: 1)genetic factors - the evidences in support are the familial aggregation; 2)racial and environmental factors - surveys in the US have revealed higher incidence of primary hypertension in blacks than in whites. A number of environmental factors have been implicated in the development of this type of hypertension including salt intake, obesity, skilled occupation, higher living standards and patients in high stress. There are some factors modifying the course of essential hypertension: A)age - younger the age at which hypertension is first noted but left untreated, B)lower the life expectancy; C)sex - females tolerate hypertension better than males; atherosclerosis - as a rule, accompanies essential hypertension. The pathogenetic mechanism are: 1) high plasma level of catecholamines; 2) increase in blood volume, i.e. arterial overfilling (volume hypertension) and arteriolar constriction (vasoconstrictor hypertension); 3) increased cardiac output;
  22. Morphology. The morphological effects of systemic hypertension are manifested as lesions in the heart, peripheral vessels, kidneys and brain. Accordingly it we distinguish several clinical and morphological types of essential hypertension. There are: 1) cardio-vascular, 2) renal, 3) cerebral.
  23. Hypertensive heart disease is an important and common form of heart disease in all world. Macroscopically, the most significant finding is marked hypertrophy of the heart, especially of the left ventricle. The weight of the heart increases to 500- 700 gm (may be 1000 gr) (normal weight is about 300 gr). The weight of the heart is directly related to the severity of hypertension but there is no correlation between the weight of the heart and duration of hypertension. The left ventricular wall is thickened (up to 20 mm or more), the papillary muscles are rounded and prominent, and the cardiac chamber is small (concentric hypertrophy). However, when decompensation and cardiac failure develop, there is eccentric hypertrophy with thinning of the ventricular wall and dilation of the left ventricular and atrial cavities. There may be dilation and hypertrophy of right heart as well. Changes in the blood vessels involve arterioles and arteries. There are 3types of these changes: 1.hyaline arteriolosclerosis that results in homogeneous and eosinophilic thickening of the wall of small blood vessels, 2.intimal thickening due to proliferation of smooth muscle cells in the intima – elastofibrosis in middle vessels – splitting of elastic membrane due to overgrowth of fibrous tissue. 3.In the large blood vessels atherosclerosis usually develops.
  24. Renal type of hypertension may be benign and malignant. Benign nephrosclerosis is the term used to describe the kidney of benign phase of hypertension. Macroscopically, both kidneys are affected equally and are reduced in size and weight, often weighing about 100 gm or less. The capsule is often adherent to the cortical surface. The surface of the kidney is finely granular and shows V-shaped areas of scarring («small contracted kidney»primarily). The cut surface shows firm kidney and narrowed cortex. Microscopically there arc primarily diffuse vascular changes, which produce parenchymal changes secondarily as a result of ischaemia, parenchymal changes. There is variable degree of atrophy of parenchyma. These include glomerular shrinkage, deposition of collagen in Bowman's space, periglomerular fibrosis. Clinical features is variable: elevation of the blood pressure with headache, dizziness, palpitation. Renal failure and uremia may occur.
  25. 1. Cerebrovascular diseases (cerebral type). Hypertension can result in two main types of parenchymal diseases of the brain: 1)ischemic brain damage (hypoxic encephalopathy and cerebral infarction); 2)intracranial hemorrhage (intracerebral and subarachnoid hemorrhage). The pathologic appearance of the brain in hypoxic encephalopathy varies depending on the duration and severity of hypoxic episode and the length of survival. Macroscopically, there is focal softening. The area supplied by distal branches of the cerebral arteries suffers from the most severe ischemic damage and may develop border zone or watershed infarcts in the adjacent zones between the territories supplied by major arteries. Microscopically, the nerve cells die and disappear and are replaced by reactive fibrillary glia. Cerebral infarction is a localized area of tissue necrosis caused by local vascular occlusion. Clinically, the signs and symptoms associated with cerebral infarction depend on the region infracted. Cerebral infarcts may be anemic or hemorrhagic. Macroscopically, an anemic infarct becomes evident 6-12 hours after its occurrence. The affected area is soft and swollen and there is blurry of junction between grey and white matter. Within 2--3 days, the infarct undergoes softening and disintegration, A hemorrhagic infarct is red and superficially resembles a hematoma. It is usually the result of fragmentation of occlusive arterial emboli or venous thrombosis. Hemorrhage into the brain of patient with hypertension, is intracerebral hemorrhage, which is usually of hypertensive origin. Most hypertensives over middle age have microaneurism in very small cerebral arteries in the brain tissue. The common sites of hypertensive intracerebral hemorrhage are the region of the basal ganglia, pons and cerebella's cortex. About 40% of patients die during the first 3-4 days of hemorrhage, mostly from hemorrhage into the ventricles. The outcome of intracerebral hemorrhage is cyst formation.
  26. The causes of death among hypertensive patients were the following:  congestive heart failure;  coronary artery disease;  cerebrovascular accidents;  uremia;  causes unrelated to hypertension. The cardiac complications therefore account for 36% of the death.
  27. Secondary hypertension may be classified as follows: 1. Renal: A) vascular diseases (coarctation (narrowing) of the aorta, atherosclerosis, arteritis, mechanical obstruction attributable to thrombosis, embolism, tumors); B) parenchymal renal diseases (glomerulo- nephritis, pyelonephritis, hydronephrosis, amyloidosis, tumors); c) perinephric diseases (perinephritis, tumors, hematoma). 2. Cerebral: a) increased intracranial pressure (trauma, inflammation, tumors); B)anxiety states; lesions of brainstem (poliomyelitis). 3.Cardiovascular: coarctation of aorta (aorta has narrow). 4.Endocrine: A) pheochromocytoma; B) adrenocortical adenomas; pituitary adenomas; C) hyperthyroidlsm. 5.Preeclampsia and eclampsia. If these causes of secondary hypertension are eliminated, hypertension disease can cured.