英文医学课件：12 13 14Diseases of the cardiovascular system(马丽琴)病理

1、Diseases of the cardiovascular system,Normal Heart,This is the external appearance of a normal heart. The epicardial surface is smooth and glistening. The amount of epicardial fat is usual. The left anterior descending coronary artery extends down from the aortic root to the apex.,The aortic valve s

2、hows three thin and delicate cusps. The coronary artery orifices can be seen just above.The endocardium is smooth, beneath which can be seen a red-brown myocardium. The aorta above the valve displays a smooth intima with no atherosclerosis.,This is the tricuspid valve. The leaflets and thin and deli

3、cate. Just like the mitral valve, the leaflets have thin chordae tendineae that attach the leaflet margins to the papillary muscles of the ventricular wall below.,This is a normal coronary artery. The lumen is large, without any narrowing by atheromatous plaque. The muscular arterial wall is of norm

4、al proportion.,This is the normal appearance of myocardial fibers in longitudinal section. Note the central nuclei and the syncytial arrangement of the fibers, some of which have pale pink intercalated disks.,Diseases,Case,案情摘要 2013年2月17日在温岭市泽国镇一出租房内发现李某，女，62岁，死在租住的出租房床上，衣着半裸；尸体解剖见多根肋骨骨折，氢化物及常规毒物检查阴

5、性。 脏器检查 心脏：重410g。大小16cm10cm8cm。左冠状动脉左前降支粥样硬化狭窄-级，冠状动脉开口处硬化。依次切开右心及左心检查：左右心室壁厚度：左1.8cm，右0.4cm；各瓣膜光滑、薄，周径分别为：三尖瓣13cm，肺动脉瓣8cm，二尖瓣10cm，主动脉瓣6cm。镜检：部分心肌纤维断裂，局部扭曲，有的纵横纹不清，部分肌细胞核肥大，有几处见纤维组织增生。间质血管扩张淤血，有处灶性出血。左冠状动脉前降支内膜增厚，其下见小灶性出血，有处钙化，管腔狭窄-级。,Case,病理诊断 左冠状动脉前降支粥样硬化、钙化伴斑块内出血，管腔狭窄-级；心脏肥大；脑基底动脉粥样硬化级； 灶性肺气肿；肝脏、

6、肾脏淤血。,Case,Case,Case,Case,Case,Case,Case,死亡原因 左冠状动脉前降支粥样硬化、钙化伴斑块内出血，管腔狭窄-级；心脏肥大。 在以上疾病存在的基础上，劳累、情绪异常、饥饱等情况下，可诱发冠状动脉痉挛，导致心肌急性缺血缺氧，心室纤维颤动而死亡。,Arteriosclerosis: thickening and inelasticity of arteries, including: Arteriolosclerosis Medial calcification Atherosclerosis,atherosclerosis(AS),1. etiology an

7、d pathogenesis Risk factors Hyperlipemia: increased LDL, TG, VLDL, apoB,Lp(a) decreased HDL,apoA-I Hypercholesterolemia Hypertriglyceridemia Hypertension Cigarette smoking Elevated blood sugar levels The other factors,Other risks: Age Sex: menopause Familial predisposition Insufficient regular physi

8、cal activity Competitive, stressful life style with type A personality behavior Obesity,Pathogenesis,-Theory of inflammatory response to injury The injury of the endothelium The accumulation of lipid The infiltration of macrophages The proliferation of SMC,T,F C,INTIMA,LUMEN,MEDIA,F C,SMC,SMC,SMC,PD

9、GF,PDGF,Smooth muscle migration and proliferation,PDGF, platelet-derived growth factor,It helps carry some of the bad cholesterol out of the body. Levels should be 35 mg/dl.,“Good” Cholesterol-HDL,LDL is known as bad cholesterol. It has a tendency to increase risk of CHD. LDLs are a major component

10、of the atherosclerotic plaque that clogs arteries. Levels should be 130 mg/dl.,“BAD” Cholesterol-LDL,(1) Ingested through the scavenger receptor (2) Chemotactic for circulating monocytes (3) Increase monocyte adhesion (4) Stimulate release of growth factors and cytokines (5) Cytotoxic to endothelial

11、 and smooth muscle cell (6) Immunogenic,Modified LDL- oxidized LDL,Endothelial injury: shear stress turbulent flow, hypoxia, smoking etc. Endothelial dysfunction Increased permeability,Cellular interactions,Monocytes/macrophages T lymphocytes Smooth muscle cells,Platelet adhering to the endothelium,

12、Monocytes entering the endothelium,2. Basic pathology,Fatty streaks: Grossly: soft, yellow intimal dots or streaks,( 3mm wide and up to 1.5cm long along the long axis of the vessel) Histologically: intimal aggregations of foam cells, derived from both macrophages and smooth muscle cells which ingest

13、 lipid with vacuolated cytoplasm. some cases undoubtedly regress,Early lipid depositions predicts thelocation of later atherosclerotic plaques,Lipid deposits in a childs aorta,From Davies, MJ, Woolf, N c Science Press,Fibrous plaques Gross: 1) Range up to several centimeters 2) Bright yellow to gray

14、 3) Raised several millimeters above the surface 4) Irregular in shape Microscopic: Small amounts of lipids; Fibrous cap: connective tissue cells with collagen and elastic fibers and proteoglycans,Atheromatous plaques GROSS: irregular in shape, yellow to gray Microscopic: Intimal surface: fibrous ca

15、p Center: an extracellular lipid core composed of cholesterol and cholesterol esters (needle-like crystals), necrotic cellular debris Margins: lipid-laden foam cells (monocyte/smooth muscle cell derived), lymphocytes Atrophy and fibrosis of the underlying media .,atheroma,These three aortas demonstr

16、ate mild, moderate, and severe atherosclerosis from bottom to top.,Cholesterol clefts are numerous in this atheroma.,This is a high magnification of the aortic atheroma with foam cells and cholesterol clefts.,Complicated lesions,Hemorrhage in plaque Rupture of the plaque or ulceration Thrombosis Cal

17、cification aneurysm: definition, lesion classification (true , pseudo-, Dissecting ),This is coronary atherosclerosis with the complication of hemorrhage into atheromatous plaque.,This is severe atherosclerosis of the aorta in which the atheromatous plaques have undergone ulceration along with forma

18、tion of overlying mural thrombus.,Ulcer formation,There is a severe degree of narrowing in this coronary artery. It is complex in that there is a large area of calcification on the lower right, which appears bluish on this H 2) Involved aortic valve ring- aortic valve disease; 3) Less luminal narrow

19、ing and thrombosis; 4) Aortic aneurysm and dissecting aneurysm.,Atherosclerotic aneurysm of the aorta in which a large bulge appears just above the aortic bifurcation. Such aneurysms are prone to rupture when they reach about 6 to 7 cm in size. They may be felt on physical examination as a pulsatile

20、 mass in the abdomen.,Coronary arteries: discuss later,Brain arteries: Circle of Willis, middle cerebral artery Ischemic disease brain atrophy and softening Aneurysmrupture hemorrhage,Thrombosis,atrophy of brain,Renal arteries: nephrosclerosis Arteries of upper and lower extremities: ischemia, claud

21、ication(跛行), gangrene Mesenteric arteries: pain, fever and so on,Fresh gangrene,Old gangrene,Coronary Atherosclerotic Heart Disease (CHD),Coronary heart disease (ischemic heart disease): Mostly due to atherosclerosis of coronary arteries A group of related syndromes caused by the imbalance between m

22、yocardial oxygen demand and blood supply,right coronary,Left coronary,Causes Coronary atherosclerosis Distribution(location) features of the lesion Spasm of the coronary arteris Coronary arteritis,Depending on the rate and severity of coronary artery narrowing and the myocardial response: Angina pec

23、toris Myocardial infarction (MI) Cardiac myosclerosis,Narrow,thrombosis,Coronary heart disease results in chest pain (angina pectoris) when lumen is focally reduced 70%.,Normal coronary segment,Atheroma,Classification 1. angina pectoris (AP) a symptom complex consisting of severe paroxymal chest pai

24、n resulting from transient ischemia,Precipitating factors Exertion, emotion, pain, cold weather, cigarette smoking, heavy meals,Angina patient,Classification Stable (exerting ) AP Instable (exerting) AP (Spontaneous) variant AP,2. Myocardial infarction Subendocardial MI Multiple small lesion Transmu

25、ral MI Distribution Morphology:shape, color, microscopic change Biochemical changes: GOT GPT CPK,Morphology,Appearance of MI: Coagulation、necrosis and inflammation (8-9h). Formation of granulation tissue and resorption of the necrotic myocardium (7d). Organization of the granulation tissue to form a

26、 fibrous scar (2-8w).,This is the left ventricular wall which has been sectioned lengthwise to reveal a large recent myocardial infarction.,myocardial infarction,granulation tissue,This cross section through the heart demonstrates the left ventricle on the left.,Complications Rupture of the heart Ve

27、ntricular aneurysm Thrombosis Acute pericarditis Clinical complication,rupture of Infarct area,In cross section, the point of rupture of the myocardium is shown with the arrow.,Pericardial tamponade,hematocele in heart sac,A cross section through the heart reveals a ventricular aneurysm with a very

28、thin wall at the arrow.,Treatment,3. Myocardial fibrosis 4. sudden coronary death,Prevention,Get regular medical checkups. Control your blood pressure. Check your cholesterol. Dont smoke. Exercise regularly. Maintain a healthy weight. Eat a heart-healthy diet. Manage stress.,Hypertension,Normal bloo

29、d pressure: systolic blood pressure (SBP)18.4kPa (140mmHg) and diastolic blood pressure (DBP)12kPa (90mmHg) Hypertension: SBP18.4kPa (140mmHg) and/or DBP12kPa (90mmHg),Essential (primary) hypertension: idiopathic hypertension 90%-95% Secondary (symptomatic) hypertension: 5%-10% Secondary to another

30、disease such as renal disease-narrowing of the renal arteries; adrenal disorders, Cushings syndrome,Normal regulation of blood pressure 1. Cardiac output blood volume heart rate left ventricular factors 2. Total peripheral resistance resistance arterioles thickness of the arteriolar wall the effect

31、of neural and hormonal influences constrict or dilate vessels,Etiology and pathogenesis:,1. Neural disorder Stress, disorder of the central regulation of BP Constrictors, dilators, peripheral resistance increasing 2. Endocrine disorder,Hypotheses,3. Renal hypotheses Renin-angiotensin-aldosterone sys

32、tem Juxtaglomerular cells Renin- ACE angiotensinogen-angiotensin1-angiotensin2 Direct action on vessel smooth muscle vasoconstriction Increases distal tubular reabsorption of sodium and water,4. Inheritable hypotheses Familial aggregation of hypertension Depend on the cumulative effects of allelic f

33、orms of several genes that affect BP 5. Other environmental factors obesity, smoking, heavy consumption of salt,Morphology (1) Benign hypertension Stage of dysfunction Stage of artery lesion arteriolosclerosisthe basic lesion of hypertension Stage of organ dysfunction heart, brain, kidney, Arteriole

34、 of eyeground,Hypertensive heart disease Concentric hypertrophy Ecentric hypertrophy Arteriolar nephrosclerosis (primary granulo-contracted kidney) Microscopic change Gross alteration,Normal heart,Concentric hypertrophy,This left ventricle is very thickened, but the rest of the heart is not greatly

35、enlarged. - Concentric hypertrophy,Eccentric hypertrophy,Kidney: hypertensive nephrosclerosis (Primary granulo-contraced kidney) Grossly: small and hard with a surface of diffuse, fine granularity; atrophic thinning of the cortex; poor demarcation of cortex from medulla on cut surface.,Microscopical

36、ly: Hyaline arteriolosclerosis: hyaline thickening of the walls of the small arteries and arterioles-narrowed lumen-decreased blood flow-ischemic atrophy Nephron: Coexisting of atrophy and hypertrophy Interstitial fibrosis and lymphocytic infiltrate Clinical feature: proteinuria,Coexisting of atroph

37、y and hypertrophy,Hyaline arteriolosclerosis is seen in the elderly, but more advanced lesions are seen in persons with diabetes mellitus and/or with hypertension.,Hypertensive brain Edema of brain, hypertensive encephalopathy, hypertensive crisis Hemorrhage of brain Softening of brain,Hemorrhages i

38、nvolving the basal ganglia area (the putamen in particular).,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.,Arteriole of eyeground,Malignant hypertension,1. Far less common, young people, kidney is the most o

39、ften affected organ. 2. Charactristic change: Fibrinoid necrosis of arterioles and arteries (necrotizing ateriolitis) Hyperplastic arterioles; an onion-skin appearance 3. Rapidly rising BP, especially DBP130mmHg,4. Necrotizing glomerulitis with micro thrombi, proteinuria, hematuria, azotemia, uremia

40、; 5. Obvious retinal(视网膜 ) changes: retinal hemorrhages and exudates, papilloedema, visual impairments, blindness 6. Most patients die of uremia, cerebral hemorrhage and cardiac failure within1-2 years without treatment.,One complication of hyperplastic arteriolosclerosis with malignant hypertension

41、 is fibrinoid necrosis, as seen here in a renal arteriole.,Malignant hypertension. The arteriole here has an onion skin appearance typical of hyperplastic arteriolosclerosis.,Etiology and pathogenesis Causes Genetic factors Environmental factors Dietary factors: Na+, Social factors psychological str

42、ess other factors,Pathogenesis Variant factorsincreased Volum, retention of Sodium and water Vasoconstriction Thickening of the artery wall,Rheumatism,Rheumatic fever is an acute, immunologically mediated, multisystem inflammatory diseases. Connective tissue disease or collagen disease.,Concept,Worl

43、dwide, an estimated 5-30 million children and young adults have chronic RHD, and 90,000 patients die from this disease each year. Most cases occur in developing countries. RF occurs in equal numbers in males and females.,Etiology and pathogenesis Infection with group A beta hemolytic streptococci Im

44、mune injury,rheumatogenic strains of group A streptococci (GAS) Evidence: 1. The onset of symptoms 2 to 3 weeks after an episode of group A streptococcol pharyngitis. It does not follow infections by streptococci at other sites, such as the skin. 2. High anti streptolysin o (ASLO) titer 3. Declined

45、remarkably over the past 30 years because of the rapid diagnosis and treatment.,Non suppurative disease-granulomatous inflammation No streptococci can be found directly in lesions. Immunologically mediated streptococci- antistreptococci cross reactions: M-protein antibodies cross-reacts to myocardiu

46、m C-antigen (glycoprotein) cross-reacts to connective tissue (joints),Basic pathology Lesions: Fibrinoid necrosis Aschoff bodies,Three stages : 1. Alteration and exudation; 1month Mucoid change Fibrinoid necrosis Cellular infiltration Lymphocytes, monocytes Plasma cells etc.,2. Proliferation or gran

47、uloma. (last 2-3 months) Characteristic lesion :Aschoff body , rheumatic body , rheumatic granuloma Location: interstitial connective tissue, especially near small blood vessels, under endocardium and skin. Shape: round or spindle,Composition: Center: fibriniod necrosis Surrounded by: chronic inflam

48、matory cells Characteristic histiocytes- Aschoff cells: large histiocytes, multinucleated, vesicular, abundant basophilic cytoplasm cross-section: owls eyes cells; longitudinal section: caterpillars cells.,Aschoff cells,Microscopically, acute rheumatic carditis is marked by a peculiar form of granul

49、omatous inflammation with so-called Aschoff nodules seen best in myocardium.,Here is an Aschoff nodule at high magnification. The most characteristic component is the Aschoff giant cell (awl-eye cell). Scattered inflammatory cells accompany them and can be mononuclears or occasionally neutrophils.,A

50、schoff cell,This is a long, thin Aschoff cell with an elongated nucleus (caterpillar cell).,Aschoff body in the heart,3. Healing or fibrous scar Fibroblast-collagen scar all stages last 4-6 months,Rheumatic heart disease is the major cause of morbidity from RF, and it is the major cause of mitral in

51、sufficiency and stenosis Rheumatic pancarditis : 1. Rheumatic endocarditis 2. Rheumatic myocarditis 3. Rheumatic pericarditis,Rheumatic endocarditis location: common; affect any valves 1 mitral valves alone, 70-75%; 2 mitral and aortic valves, 25% 3 other valves,Lesions: gross 1. Edematous and thick

52、ened valves; 2. Formation of small, grey vegetations along the lines of valve closure- verrucous endocarditis 3. Leaflet thickening, fusion and shortening, and thickening and fusion of the tendinous cords,Microscopically: 1. Foci of fibrinoid necrosis, but Aschoff bodies are not common 2. Vegetation

53、s consist of fibrin and platelets,Acute rheumatic mitral valvulitis. Small vegetations are visible along the line of closure of the mitral valve leaflet (arrows).,Chronic rheumatic myocarditis. The mitral valve leaflets are thickened, opaque and fused at the commissures. The chordae tendineae are al

54、so thickened and shortened as a result of fibrosis.,In time, chronic rheumatic valvulitis may develop by organization of the acute endocardial inflammation along with fibrosis, as shown here affecting the mitral valve. Note the shortened and thickened chordae tendineae.,Prognosis 1. The acute change

55、s may resolve without severe scarring and chronic valvalar deformities. 2. The repeat lesions make the valves fibrous thicken and adherent, chordae tendineae thicken and shorten.,Rheumatic myocarditis Stromal connective tissue edema, fibrinoid necrosis, Aschoff bodies, scar. The myocardium may also

56、contain diffuse interstitial edema and inflammatory infiltrates, these cause cardiac failure, especially in children.,Rheumatic pericarditis Fibrinous pericarditis（纤维素性心包炎） Cor villosum(绒毛心): organization, adhesion Constrictive pericarditis（缩窄性心包炎）,The epicardial surface of the heart shows a shaggy

57、fibrinous exudate. An example of fibrinous pericarditis.,Changes of other organs,(1) Rheumatic arthritis 1. large joints: wrists, elbows, ankles, knees; 2. Migratory（游走性） polyarthritis; 3. stiffness, swelling, pain 4. chronic inflammatory infiltrates and edema sometime Aschoff bodies in the involved

58、 joints and periarticular soft; 5. self-limited, do not cause chronic deformity.,(2) Rheumatic arteritis Coronary, renal, mesenteric and cerebral arteries as well as aortic and pulmonary vessels. Wall of vessels: edema, fibrinoid necrosis, inflammatory cells infiltration, Aschoff bodies, fibrious scar.,(3) Skin change exudation lesion: erythema marginatum proliferation lesion: subcutaneous nodules,(4) Rheumatic lesion of central nerve system 5-12 year old children rheumatic arteritis neuron degeneration proliferation of microglia cells chorea minor-non-progressiv