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Disease of the Cardiac-Vascular System PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "DISEASES OF THE CARDIAC-VASCULAR SYSTEM" by T. Filonenko.

This medical PowerPoint presentation talks about cardiovascular diseases (CVDs). The cardiovascular system includes the heart, blood vessels, and blood. Diseases that affect this system are called cardiovascular diseases (CVDs) and can range from mild to life-threatening. Some common diseases of the cardiovascular system include Coronary artery disease (CAD), Hypertension (high blood pressure), Heart failure, Arrhythmias, Atherosclerosis, Heart valve disease, Cardiomyopathy, Peripheral artery disease (PAD), and Stroke.

Tags : cardiovascular diseases, CVDs, cardiovascular system, Coronary artery disease, CAD, Hypertension, high blood pressure, Heart failure, Arrhythmias, Atherosclerosis, Heart valve disease, Cardiomyopathy, Peripheral artery disease, PAD, Stroke, cardiology

Published on : Mar 17, 2023 | Views : 1703 | Downloads : 3

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DISEASES OF THE CARDIAC-VASCULAR SYSTEM Lecture on pathomorphology for the 3-rd year students by T. Filonenko
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Atherosclerosis Atherosclerosis is a chronic disease affecting primarily the intima of large and medium-sized muscular arteries and characterized by fibro-fatty plaques or atheromas
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The major background factors Age Sex Genetic factors (familial hypercholesteronemia) Geographic factors Diet Hypertension Metabolic diseases: diabetes mellitus, myxedema, nephrosis, xanthomatosis Cigarette smoking Lack of physical exercise. Other risk factors (such as obesity, hyperglycemia, stress, coffee consumption)
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A. Endothelial injury is accompanied by the attachment of monocytes, platelets, and thrombus formation. B. Macrophages in the intima phagocytise lipid and transform into foam cells. Macrophages also secrete growth factors that stimulate the proliferation of smooth muscle cells. C. Ruptured atheromas release thrombogenic material into the circulation, causing thrombus for intimal ulceration. Pathogenesis of Atherosclerosis
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Microscopical stages of atherosclerosis Pre-lipid stage Stage of fatty stripes Stage of liposclerosis Stage of atheromatosis Stage of ulceration Stage of atherocalcinosis
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Early lesions of atherosclerosis Accumulations of fat in intima. Intimal plaque composed of foamy cells and proliferated smooth muscle cells
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Many foam cells (macrophages and proliferated smooth muscle cells full of lipid material) and a cholesterol cleft are recognized by their typical needle-shaped appearance. Progressing phase
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Late ulcerative stage There is a severe degree of narrowing in this coronary artery. It is "complex" in that there is a large area of calcification. Complex atheroma have calcification, thrombosis, or hemorrhage. Such calcification would make coronary angioplasty difficult.
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Clinical-morphological appearences Atherosclerosis of aorta Atherosclerosis of coronary arteries of heart Atherosclerosis of cerebral arteries Atherosclerosis of renal arteries Atherosclerosis of mesenteric arteries Atherosclerosis of femoral arteries
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Atherosclerosis of aorta Here, the dissection went into the muscular wall. Atherosclerosis may weaken the wall of the aorta such that it bulges out to form an aneurysm. An atherosclerotic aortic aneurysm typically occurs in the abdominal portion below the renal arteries. Aortic aneurysms that get bigger than 6 or 7 cm are likely to rupture.
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Atherosclerosis of coronary arteries Here is a coronary artery with atherosclerotic plaques. There is hemorrhage into the plaque. This is one of the complications of atherosclerosis. Such hemorrhage could acutely narrow the lumen.
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Atherosclerosis of cerebral arteries Atherosclerosis with thrombus of the internal carotid artery is seen here.
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Atherosclerosis of renal arteries Atherosclerosis of renal artery can lead to renal infarction or to development of scars or atrophy of kidney
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Atherosclerosis of mesenteric arteries Hemorrhagic infarct and gangrene of small intestine
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This is gangrene of the lower extremity ( "dry" and "wet" gangrene) due to loss of blood supply. Gangrenous necrosis involves the tissues of a body part. Because multiple tissues are non-viable, amputation of such areas is necessary. Atherosclerosis of femoral arteries
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Clinical effects Slow luminal narrowing causing ischemia and atrophy Sudden luminal occlusion causing infarction Propagation of plaque by formation of thrombi and emboli Formation of aneurism and eventual rupture
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Hypertension Arterial hypertension is defined clinically as borderline when it riches 140/90 mm Hg and hypertensive when 165/95 mm Hg.
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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. 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 hemorrhages and hypertensive encephalopathy.
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Background factors to essential hypertension genetic factors environmental factors including salt intake, obesity, skilled occupation, higher living standards and patients in high stress age sex atherosclerosis The pathogenetic mechanisms 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; 4) low-renin essential hypertension found in approximately 20% patients due to decreased responsiveness to renin release; 5) high renin essential hypertension due to decreased adrenal responsiveness to angiotensin 2
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Classification depending on stage of hypertensive disease. Subclinical stage occurs by hypertrophy of muscular layer and elastic structures of arterioles and small-sized arteries, spasm of arterioles. The stage of general changes of arteries begins as arterial pressure increases. The stage of secondary changes of organs.
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Morphological changes Hypertrophy of muscular layer and elastic structures of arterioles and small-sized arteries, spasm of arterioles. Small muscular arteries show segmental dilatation as a result of necrosis of smooth muscle cells. Fibrinoid necrosis.It is the combination of cell necrosis and deposition of plasma proteins in the vessel wall. Proliferation and a striking increase in the number of layers of smooth muscle cells, so-called onion-skin appearance. Arteriosclerosis, elastofibrosis and hylinosis. Circular atherosclerosis.
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The main clinical-morphological types of essential hypertension Cardiac type Cerebral type Renal type
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Hypertrophy of the myocardium occurs. Weight of heart reaches 1 kg, thickness of left ventricle walls is up to 3 cm. Heart is called “cor bovinum”. Ischemic heart disease (IHD). Cardiac type In eccentric hypertrophy (hypertrophy and dilation), the heart is decompensated
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The large hemorrhage in this adult brain arose in the basal ganglia region of a patient with hypertension. This is one cause for a "stroke". Cerebral type
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In malignant nephrosclerosis, the kidney demonstrates focal small hemorrhages. This is due to an accelerated phase of hypertension in which blood pressures are very high (such as 300/150 mm Hg). Renal type Sometimes the small arteries and arterioles can be damaged so severely in malignant hypertension that they demonstrate necrosis with a pink fibrin-like quality that gives this process its name--fibrinoid necrosis.
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Here is an example of renal vascular disease known as benign nephrosclerosis. The smaller arteries in the kidney have become thickened and narrowed. Hyaline arteriolosclerosis with hypertension is present. It can lead to patchy ischemic atrophy with focal loss of parenchyma that gives the surface of the kidney the characteristic granular appearance as seen here. It is called “primary shrunken kidney”. Thickening of the arterial wall with malignant hypertension also produces a hyperplastic arteriolitis. The arteriole has an "onion skin" appearance.
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The end result of many renal diseases--whether they are renal vascular diseases, glomerulonephritis, or chronic pyelonephritis--is end stage renal disease. In end stage renal disease, the kidneys are small bilaterally, as shown here. This condition is associated with chronic renal failure, and the patient's creatinine are elevated. Chronic renal failure can be treated by dialysis or by transplantation, as shown here. The microscopic appearance of the "end stage kidney“. The cortex is fibrotic, the glomeruli are sclerotic, there are scattered chronic inflammatory cell infiltrates, and the arteries are thickened.
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What is Ischemic Heart Disease? Ischemic heart disease is caused by an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. Reduction in coronary blood flow is related to progressive atherosclerosis with increasing occlusion of coronary arteries. Blood flow can be further decreased by superimposed events such as vasospasm, thrombosis, or circulatory changes leading to hypoperfusion.
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Decreased aortic diastolic pressure Increased intraventricular pressure and myocardial contraction Coronary artery stenosis, which can be further subdivided into the following etiologies: Fixed coronary stenosis Acute plaque change (rupture, hemorrhage) Coronary artery thrombosis Vasoconstriction Aortic valve stenosis and regurgitation Increased right atrial pressure Factors reducing coronary blood flow
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1. Angina pectoris - a symptom complex of IHD characterized by paroxysmal attacks of chest pain, usually substernal or precordial, caused by myocardial ischemia that falls short of inducing infarction. There are several patterns: Stable angina (typical) Variant or Prinzmetal's angina Unstable angina Sudden cardiac death 2. Myocardial Infarction (MI) 3. Ischemic Cardiomyopathy Patterns of Ischemic Heart Disease (IHD)
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Sudden cardiac death is defined as death occurring within an hour of onset of symptoms. Such an occurrence often complicates ischemic heart disease. Such patients tend to have severe coronary atherosclerosis (>75% lumenal narrowing). Often, a complication such as coronary thrombosis or plaque hemorrhage or rupture has occurred. The mechanism of death is usually an arrhythmia.
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Occlusive intracoronary thrombus - a thrombus overlying an ulcerated or fissured stenotic plaque causes 90% of transmural acute myocardial infarctions. Vasospasm - with or without coronary atherosclerosis and possible association with platelet aggregation. Emboli - from left sided mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale. The pathogenesis of Myocardial Infarction (MI)
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Patterns include: Transmural infarct - involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%. Isolated infarcts of RV and right atrium are extremely rare. Subendocardial infarct - multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall. These do not show the same evolution of changes seen in a transmural MI. The gross appearance of a myocardial infarction can vary.
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Gross morphologic changes evolve over time as follows:
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Arrhythmias and conduction defects, with possible "sudden death" Extension of infarction, or re-infarction Congestive heart failure (pulmonary edema) Cardiogenic shock Pericarditis Mural thrombosis, with possible embolization Myocardial wall rupture, with possible tamponade Papillary muscle rupture, with possible valvular insufficiency Ventricular aneurysm formation Complications of Myocardial Infarction
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There may be previous myocardial infarction (postinfarctional cardiosclerosis) Severe coronary atherosclerosis involving all major branches (diffuse cardiosclerosis). The result is an inadequate vascular supply which leads to myocyte loss, fibrosis, hypertrophy, development of aneurism. Cardiac dilation results in overload of remaining myocytes. This keeps the process going, with compensation by continuing myocyte hypertrophy. Eventually, the heart can no longer compensate, and cardiac failure ensues with arrhythmias and/or ischemic events. Thus, clinically, there is slow, progressive heart failure with or without a history of a previous MI or anginal pain. Ischemic cardiomyopathy is responsible for as much as 40% of the mortality in IHD. Ischemic Cardiomyopathy