高血压英文ppt精品课件cardiovascular

Introduction to Cardiovascular Pathology - Fred Clayton,Systemic Pathology of Congestive Heart Failure Pathology of Myocarditis Pathology of Cardiomyopathy Dilated Cardiomyopathy Hypertrophic Cardiomyopathy Restrictive Cardiomyopathy,Congestive Heart Failure,Cardiac output insufficient for metabolic requirements of the body Systolic dysfunction decreased myocardial contractility Diastolic dysfunction insufficient expansion for ventricular volume Problems are accentuated by increased demand high output heart failure,CHF Bodys Compensation,Tachycardia Frank-Starling increased End Diastolic Volume Myocardial hypertrophy Renin-angiotensin-aldosterone system Catecholamines positive inotropic effect Adrenergic redistribution of blood flow Increase oxygen extraction from hemoglobin,Left-sided Heart Failure,Ischemic heart disease Hypertension Aortic and mitral valve disease Myocardial disease,Lungs Pulmonary edema,Dyspnea breathlessness Orthopnea dyspnea lying down Paroxysmal nocturnal dyspnea extreme dyspnea,Lung Pulmonary Edema pale pink edema fluid filling alveoli,Lung alveolar hemorrhage, heme-filled macrophages “heart failure cells”, with iron stain to right,Kidneys reduced perfusion,Ischemic tubular necrosis / ATN Prerenal azotemia,Kidney -ATN,Brain in CHF cerebral hypoxia,Irritability Loss of attention span Restlessness Stupor Coma,Right-sided heart failure,Pure cor pulmonale Consequence of left-sided failure Myocardial myocarditis, cardiomyopathy, constrictive pericarditis,Right failure - systemic effects,Liver chronic passive congestion Spleen congestive splenomegaly Kidneys congestion and hypoxia Sub-Q peripheral edema and anasarca Pleural space effusions Brain venous congestion and hypoxia Portal - ascites,Liver chronic passive congestion blood pools near the central veins,Liver chronic passive congestion,Liver chronic passive congestion blood pools near the central veins,Liver chronic passive congestion red cell pooling near central veins and pericentral necrosis of the hepatocytes,CHF final pathway to death,Ischemic heart disease Hypertensive heart disease Valvular heart disease Cardiomyopathy Myocarditis Specific heart muscle diseases,Myocarditis Etiology,Viral Coxsackie A, ECHO, Influenza Chlamydia and Rickettsia psittaci & typhi Bacteria diphtheria, TB, Strep Fungal & Protozoa Trypanosomes, Toxo Hypersensitivity SLE, RHD, drugs Physical Agents Radiation Idiopathic Giant cell myocarditis,Myocarditis Morphology,Gross dilated, flabby heart, pale patches with hemorrhage Microscopic interstitial inflammatory infiltrate with myocyte necrosis, fibrosis Mononuclear cells idiopathic or viral Neutrophils bacterial Eosinophils hypersensitivity or protozoa Granulomatous TB or sarcoid,Dilated, globoid heart in myocarditis,Myocarditis meets Dallas criteria of a T lymphocyte infiltrate and myocyte necrosis or dropout. This is usually either viral or of unknown cause.,Diphtheria myocarditis due to a toxin rather than bacterial invasion. There is some inflammation, myocyte changes (see the big nucleolus). Myocyte necrosis (not shown) also happens.,Bacterial colony in myocarditis,Toxoplasmosis,Chagas disease,Giant Cell Myocarditis,Myocyte necrosis Multinucleated giant cells Lymphocytes, plasma cells, macrophages, eosinophils, and neutrophils Often fulminant, rapid progression to death Differential diagnosis cardiac sarcoidosis,Giant Cell Myocarditis,Giant Cell Myocarditis,Cardiomyopathies,Dilated Cardiomyopathy,Gross increased weight, dilatation, endocardial fibrosis, normal valves and coronary arteries Microscopic myocyte hypertrophy, myofibrillar loss and interstitial fibrosis Etiology viral, genetic, toxins Clinical significance heart failure & death,Dilated cardiomyopathy,Cardiomyopathy loss of myofibrils,Cardiomyopathy trichrome stain showing extensive fibrosis (blue) between the myocytes. The myocytes also vary in size, and some have partial loss of myofibrils.,Normal Heart - EM,Loss of fibrils in cardiomyopathy. The myocyte at lower left is about normal; the others have an extensive loss of myofibrils.,Cardiomyopathy loss of fibrils and a small contraction band in the top center.,Hypertrophic Cardiomyopathy,Hypertrophy of ventricular septum (95%) Disarray of myofibers (100%) Volume reduction of ventricles (90%) Endocardial thickening of LV (75%) Mitral valve leaflet thickening (75%) Dilated atria (100%) Abnormal intramural coronaries (50%),Hypertrophic cardiomyopathy,Hypertrophic cardiomyopathy,Hypertrophic cardiomyopathy,Hypertrophic cardiomyopathy myofiber dysarray not all fibers are pulling the same direction. Thus the contraction is ineffective. However, the cardiac conduction system can have these same problems, which might cause the arrhythmias and sudden death these patients tend to die of.,Hypertrophic Cardiomyopathy,Etiology hereditary, mostly autosomal dominant, can appear sporadically Clinical significance syncope, arrhythmias and sudden death with a risk of 2-6% per year Cannot equate with hypertrophy alone! There is variation in heart size without disease. Large hearts correlate with endurance (Secretariat, Lance Armstrong).,Restrictive Cardiomyopathy,Amyloidosis Endomyocardial fibrosis subendocardial fibrosis Loefflers endocarditis eosinophilic infiltrate Endocardial fibroelastosis,Amyloidosis notice the pink material between the myocytes.,Amyloidosis Congo Red is very, very positive.,Amyloidosis this heart is thickened, pale, and has a rubbery consistency that interferes with cardiac expansion during diastole.,Endomyocardial fibrosis fibrosis under the endocardium and in the the inner third of the myocardium.,Endomyocardial fibrosis of a ventricular wall. When extensive, this would cause restrictive heart failure too.,Endocardial fibroelastosis elastic stain (black) is very positive. This disease, which occurred in young children and was once 1:5,000 births, now is almost never seen. Etiology is not known (? viral such as mumps).,Endocardial fibroelastosis,Specific Heart Muscle Diseases,Toxic alcohol, catecholamines, cocaine, Adriamycin Metabolic hemochromatosis, hyperthyroidism Neuromuscular muscular dystrophy Storage disease glycogen, Fabrys disease Infiltrative - sarcoidosis,Heart - Beckers muscular dystrophy looks like idiopathic dilated cardiomyopathy.,Note the fibrosis and loss of myofibrils in some cells.,By electron microscopy, this was Adriamycin toxicity. See the clear vacuoles (they are dilated sarcoplastic reticulum) and severe loss of myofibrils.,Cocaine heart necrosis with contraction bands. This could happen with any severe chronic stimulation such as too much pressors in a failing heart or a