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Diseases of the cardiovascular system Maliqin Department of Pathology and Pathophysiology School of Medicine, Zhejiang University
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atherosclerosis(AS) 1. etiology and pathogenesis Risk factors Hyperlipemia:increased LDL, TG, VLDL, apoB,Lp(a) decreased HDL,apoA-I Hypertension Cigarette smoking Elevated blood sugar levels The other factors
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pathogenesis --Theory of inflammatory response to injury The injury of the endothelium The accumulation of lipid The infiltration of macrophages The proliferation of SMC
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2.morphology Predilection for large arteries and medium-sized arteries Basic lesion Fatty streak Accumulated lipid, foam cell Fibrous plaque-- Fibrous cap
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黄色脂 质条纹
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2.morphology Predilection for large arteries and medium-sized arteries Basic lesion Fatty streak Accumulated lipid, foam cell Fibrous plaque-- Fibrous cap
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动脉管壁一侧明显增厚
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Atheromatous plaque (atheroma ) Fibrous cap cholesterol crystal necnotic debris foam cell calcification neovascular formation
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atheroma
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complicated lesions Hemorrhage in plaque Rupture of the plaque Thrombosis Calcification aneurysm: definition, lesion classification (true, pseudo-, Dissecting )
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Ulcer formation
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3. Atherosclerosis of the important organs Aorta: abdominal aorta Coronary arteries Arteries of the brain The other organs
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3. Atherosclerosis of the important organs Aorta: abdominal aorta Coronary arteries Arteries of the brain The other organs
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基底动脉内血 栓形成 基底动脉 环硬化
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脑动脉 硬化致 脑萎缩
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3. Atherosclerosis of the important organs Aorta: abdominal aorta Coronary arteries Arteries of the brain The other organs
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Coronary heart disease (C H D) Definition cardiac disease which result from insufficient coronary blood flows due to the narrowing of the coronary arteries
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Causes Coronary atherosclerosis Distribution(location) features of the lesion Spasm of the coronary arteris Coronary arteritis
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正常心脏
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左冠状动脉 右冠状动脉
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正常冠状动脉
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冠状动 脉粥样 硬化, 管腔狭 窄
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冠状动脉管壁增厚及钙化 ,管腔明显狭窄
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斑块内钙化
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动脉管腔狭窄血栓形成
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冠状动脉 近端狭窄 冠状动脉 远端闭塞
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冠状动脉 硬化区
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冠状动脉阻塞冠状动脉阻塞
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Causes Coronary atherosclerosis Distribution(location) features of the lesion Spasm of the coronary arteris Coronary arteritis
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Classification 1. angina pectoris (AP) a symptom complex consisting of severe paroxymal chest pain resulting from transient ischemia
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Precipitating factors Exertion, emotion, pain, cold weather, cigarette smoking, heavy meals
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Classification Stable (exerting ) AP Instable (exerting) AP (Spontaneous) variant AP
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2. Myocardial infarction Subendocardial MI Multiple small lesion Transmural MI Distribution Morphology:shape, color, microscopic change Biochemical changes:
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myocardial infarction granulation tissue
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Complications Rupture of the heart Ventricular aneurysm Thrombosis Acute pericarditis Clinical complication
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rupture of Infarct area
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Pericardial tamponade
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hematocele in heart sac
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vntricular aneurysm
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3. Myocardial fibrosis 4. sudden coronary death
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Hypertension Diagnostic criteria sustained diastolic pressure above 90 mmHg and/or sustained systolic pressure above 140mmHg
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Classification Primary(essential) hypertension Secondary(symptomatic) Benign (chronic) hypertension Malignant(accelerated)
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Morphology (1) Benign hypertension Stage of dysfunction Stage of artery lesion arteriolosclerosis — the basic lesion of hypertension Stage of organ dysfunction
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Hypertensive heart disease Concentric hypertrophy Ecentric hypertrophy Arteriolar nephrosclerosis (primary granulo-contracted kidney) Microscopic change Gross alteration
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concentric hypertrophy of left ventricle
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decompensation distention of left ventricle
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Hypertensive heart disease Concentric hypertrophy Ecentric hypertrophy Arteriolar nephrosclerosis (primary granulo-contracted kidney) Microscopic change Gross alteration
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Hypertensive brain Edema of brain, hypertensive encephalopathy, hypertensive crisis Hemorrhage of brain Softening of brain Lesions of retina
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Arteriole of eyeground
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(2) Malignant hypertension Basic lesion: necrotic arteriolitis proliferating arteriosclerosis The major injured organs: kidney and brain
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Etiology and pathogenesis Causes Genetic factors Environmental factors Dietary factors: Na+, K+,Ca2+ Social factors psychological stress other factors
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Pathogenesis Variant factors — increased Volum, or Increased vasoconstriction retention of Sodium and water Vasoconstriction Thickening of the artery wall
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Cardiomyopathy Classification: The common lesion: Primary cardiomyopathy Any dysfunction of the myocardium not attribulable to CHD,valvular disease, hypertension or pulmonary heart disease.
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Dilated cardiomyopathy Hypertrophy(M>350g F>300g) Dilatation of the four cavities Heart failure
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Microscopically, the heart in cardiomyopathy demonstrates hypertrophy of myocardial fibers (which also have prominent dark nuclei) along with interstitial fibrosis.
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Here is a large, dilated left ventricle typical of a dilated, or congestive, cardiomyopathy. Many of these have no known etiology (so-called "idiopathic dilated cardiomyopathy") while others may be associated with chronic alcoholism. The heart is very enlarged and flabby.
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Hypertrophic cardiomyopathy Hypertrophy of the myocardium Asymetric hypertrophy of the ventricular septum Obstruction of the outflow tract
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There is marked left ventricular hypertrophy, with asymmetric bulging of a very large interventricular septum into the left ventricular chamber. This is hypertrophic cardiomyopathy.
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Restrictive cardiomyopathy progressive fibrosis of the endocardium and subendocardial myocadium
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This section of myocardium demonstrates amorphous deposits of pale pink material between myocardial fibers. This is characteristic for amyloid. Amyloidosis is a cause for "infiltrative" or "restrictive" cardiomyopathy. It is a nightmare for anesthesiologists when intractable arrhythmias occur during surgery on such patients.
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KeShan disease Etiology Virus infection Coxsackie B Lack of Selennium Morphology Dilatation of the left and right ventricle
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Rheumatism Etiology and pathogenesis Infection with group A beta hemolytic streptococci Immune injury
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Basic lesion(three stages) Alterative and exudative phase Mucoid degeneration fibrinoid necrosis Proliferative phase (granulomatous phase )
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Aschoff body (consist of) Fibrinoid necrosis Aschoff cell:awl-eye cell, caterpillar cell Aschoff giant cell Other inflammatory cells Fibrosis phase
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Aschoff body (consist of) Fibrinoid necrosis Aschoff cell:awl-eye cell, caterpillar cell Aschoff giant cell Other inflammatory cells Fibrosis phase
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Rheumatic heart disease Rheumatic endocarditis (verrucous endocarditis) Distribution: mitral valve 50% mitral and aortic valve 50% Lesion: vegetations sequla: valvular disease, MacCallum ’ s plaque
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Rheumatic myocarditis Adults: local stromal myocarditis Children:diffuse stromal myocarditis Rheumatic pericarditis dry pericarditis wet pericarditis Clinical course
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rheumatic myocarditis
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rheumatic granulomas
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Aschoff cell
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Rheumatic myoicarditis Adults: local stromal myocarditis Children:diffuse stromal myocarditis Rheumatic pericarditis dry pericarditis wet pericarditis Clinical course
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Rheumatic arthritis Large joints, reversible Rheumatic lesion of the skin Erythema annullare Subcutaneous nodules Rheumatic arteritis
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Rheumatic encephalopathy Rheumatic arteritis of the brain Rheumatic encephalitis Chorea minor
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Chronic valvular vitium of the heart stenosis, insufficiency Mitral stenosis The valvular changes The cardiac changes The clinical course
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风湿性心瓣膜病 左房扩张
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左房扩张 瓣膜硬化 左室萎缩
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二尖瓣 膜及腱 索增厚 变硬
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二尖瓣 狭窄 左心房 扩张
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Mitral insufficiency The valvular changes The cardiac changes The clinical course Aortic stenosis and insufficiency
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Subacute infective endocarditis(SBE) Etiology Streptococci. Morphology vegetations
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Vegetations(compared with rheumatic valvitis) Large, yellow, located haphazardly, located at the margin of the valve containing causative organism friable
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亚急性 细菌性 心内膜 炎
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赘生物 瓣膜病 变
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Complication Septicemia Embolism Immune injury
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Myocarditis Etiology Morphology Viral myocarditis Bacterial myocarditis Isolated myocarditis Clinical course
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The interstitial lymphocytic infiltrates shown here are characteristic for a viral myocarditis, which is probably the most common type of myocarditis.
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Thank you!
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