Diseases of cardiavascular system

Transcription

1 Diseases of cardiavascular system Ph.D Wei Zhang ( 张伟 ) Associate Professor Institute of Pathology & Forensic Medicine, Zhejiang University, School of Medicine zwei72@zju.edu.cn

2 Hypertension Introduction (Definition, Criteria, classification) Etiology & Pathogenesis Morphology

3 Hypertension Definition (WHO/ISH): A sustained rise of the systemic blood pressure systolic blood pressure (SBP) 140mmHg and/or diastolic blood pressure (DBP) 90mmHg

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5 Classification Essential (primary ) hypertension : idiopathic hypertension 90%-95% secondary ( symptomatic) hypertension : 5%-10% secondary to another disease such as renal disease, narrowing of the renal arteries; adrenal disorders, primary aldosteronism, cushing s syndrome

6 Etiology Genetic factors: family history Enviromental factors: Diet-high intake of sodium Lifestyle-stressful Weight- obesity Alcohol-increased intake Smoking inactivity

7 pathogenesis normal regulation of blood pressure 1. Cardiac output blood volume heart rate contractility 2.Total peripheral resistance neural factors hormonal factors local factors

8 pathogenesis

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10 complex disorder more than one cause may be initiated by disturbances in any of the factors act in genetically predisposed individual

11 Hypertension: Signs & Symptoms Early stages is asymptomatic or vague Fatigue Malaise morning headaches Later: stroke, heart failure, renal failure

12 Classification Benign Hypertension Malignant Hypertension

13 Pathology 一. benign or chronic hypertension (95%) remains at a modest level ; fairly stable over years to decades; Compatible with long life unless an MI or cerebrovascular accident supervenes. 1. Functional changes of vessels (first stage) arterial discontinuous spasm; fluctuating BP change; no obviously clinical feature.

14 2.structure changes of vessels 1). hyaline arteriole arterial continuous spasm--increased permeability of the small vessels-- endothelial injury--plasma proteins deposition microscopically vessel wall replaced by homogenous eosinophilic material; Reduction of luminal diameter.

15 2). muscular arteries progressive thickening of their walls hypertrophy of the muscular media and later fibrosis; fibroelastic hyperplasia high increasing BP; obviously clinical features.

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17 Renal arteriolosclerosis: homogenous, pink and hyaline deposition within the wall

18 Renal arteriolosclerosis

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20 3. organ changes ( third stage ) 1)heart : hypertensive heart disease Diagnostic principle: history of chronic hypertension left ventricular hypertrophy except for that caused by other disease.

21 compensation : concentric hypertrophy grossly : large size, heavy weight, thickened wall and papillary muscles microscopically : hypertrophy of myocardium enlarge nuclei decompensation : eccentric hypertrophy ventricular dilatation cardiac failure(left right)

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27 2) kidney : arteriolar nephrosclerosis or primary granulo-contracted kidney grossly: small and hard with a surface of diffuse, fine granularity; cut surface : atrophic thinning of the cortex; poor demarcation of cortex from medulla.

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29 microscopically: hyaline arteriolosclerosis: hyaline thickening of the walls of the small arteries and arterioles--narrowed lumen--decreased blood flow--- ischemic atrophy nephron: some atrophy some hypertrophy interstitial fibrosis and lymphocytic infiltrate. clinical feature: proteinuria

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34 3) brain Cerebral edema: hypertensive encephalopathy: severe cerebral edema sharprising of blood pressure functional disorders of CNS. clinical features: increase in intracranial pressure, headache, vomiting hypertensive crisis: more severe clinical features such as clouding of consciousness, death Softening of the brain: Cerebral hemorrhages: most fatal complication most locations: basal nucleus; internal capsule

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37 4)retinal changes Grade1 silver wiring of the arteries Grade3 retinal hemorrhages and exudations, papilloedema; visual impairments

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39 二. malignant hypertension 1. Far less common, young people; 2.charactristic change : necrotizing arteriolitis (fibrinoid necrosis) hyperplastic arteriolosclerosis: an onion-skin appearance 3.rapidly rising BP especially DBP 130mmHg

40 necrotizing glomerulitis with microthrombi proteinuria, hematuria, azotemia, uremia; obvious retinal changes retinal hemorrhages and exudates, papilloedema, visual impairments,blindness Most patients die of uremia,cerebral hemorrhage and cardiac failure within 1-2 years without treatment.

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47 Rheumatism 一. Concept An immunologically mediated, multisystem inflammatory disease, which mainly invade the body connective tissue. It is characterized by formation of rheumatic granuloma. That follows an episode of group A hemolytic streptococcal infection after an interval of a few weeks.

48 Clinical featrues Fever(Rheumatic Fever) Carditis Polyarthritis Erythema Marginatum &Erythema Nodosum ASO

49 Epidemiology 5-15(6-9)yrs Male=Female China: West>East North>South the Winter & the Spring

50 Etiology and pathogenesis relates to infection of group A, b-hemolytic streptococci Evidence: 1. the onset of symptoms 2 to 3 weeks after infection and the absence of streptococci 2. High antistreptolysin o (ASO) titer 3. Declined remarkably over the past 30 years because of the rapid diagnosis and treatment of streptococcol pharyngitis.

51 4. Nonsuppurative disease no streptococci can be found directly in lesions. Pathogenesis: Cross-reaction of the Abs against Protein M with normal proteins present in the heart, joints, & other tissues.

52 Basic pathology basic lesions: fibrinoid necrosis Aschoff bodies Granulomatous Inflammation

53 three stages : 1. Alterative and exudative phase 2. Proliferative phase 3. Healed phase

54 1. Alteration and exudation (1 month) mucoid change fibrinoid necrosis cellular infiltration lymphocytes, monocytes, plasma cells etc.

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56 2. Proliferation or granuloma (last 2-3 months) characteristic lesion Aschoff body, rheumatic granuloma location : interstitial connective tissue of myocardium, especially near small blood vessels. Under endocardium and skin. shape : round or spindle

57 composition : central focus : fibriniod necrosis surrounded by : chronic inflammatory cells and Aschoff cells Aschoff cells :large histiocytes, abundant basophilic cytoplasm cross-section : awl-eye cells; longitudinal section : caterpillar cells.

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59 Aschoff bodies

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61 Aschoff body

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64 3. Healing or fibrous scar ( Last 2-3 months) fibroblast cells collagen scar all stages last 4-6 months

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67 RHEUMATIC PATHOLOGY IN THE ORGANS Rheumatic Carditis Rheumatic Arthritis Skin Rheumatic Nodule Rheumatic Vasculitis Brain Sydenham Chorea

68 二. Rheumatic heart disease Rheumatic carditis: 1. Rheumatic endocarditis 2. Rheumatic myocarditis pancarditis 3. Rheumatic pericarditis

69 ( 一 ) rheumatic endocarditis location: affect any valves 1.mitral valves alone, 70-75%; 2. mitral and aortic valves, 25% 3.other valves

70 lesions: G: 1. edematous and thickened valves; 2. formation of small, grey vegetations along the lines of valve closure verrucous endocarditis M: 1.foci of fibrinoid necrosis, but Aschoff bodies are not common 2.vegetations consist of fibrin and platelets-----pale thrombus

71 Prognosis 1. The acute changes may resolve without severe scarring and chronic valvular deformities. 2. The repeat lesions make the valves fibrous thicken and adherent, chordae tendineae thicken and shorten.

72 McCallum plaque lesions of orgnization thickened and rough endocardium especially in the posterior wall of left atrium thrombosis

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80 ( 二 ) Rheumatic myocarditis stromal connective tissue; edema, fibrinoid necrosis, Aschoff bodies, scar. Sometimes,the myocardium may also contain diffuse interstitial edema and inflammatory infiltrates, these cause cardiac failure especially happen in children.

81 ( 三 ) Rheumatic pericarditis Fibrinous exudation: fibrinous pericarditis cor villosum : orgnization, adhesion constrictive pericarditis Serous exudation:

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83 三. Changes of other organs ( 一 ) Rheumatic arthritis 1. large joints : wrists, elbows, ankles, knees; 2. migratory polyarthritis; 3. stiffness, swelling, pain 4. chronic inflammatory infitrates and edema sometimes Aschoff bodies in the involved joints and periarticular soft tissue; 5. self-limited, do not cause chronic deformity.

84 ( 二 ) Rheumatic arteritis coronary, renal, mesenteric and cerebral arteries as well as aortic and pulmonary vessels. Wall of vessels : edema, fibrinoid necrosis, imflammatory cells infiltration, Aschoff bodies, fibrous scar.

85 ( 三 ) skin and subcutaneous tissue change exudation lesion : erythema marginatum proliferation lesion : subcutaneous nodules ( 四 )rheumatic lesion of central nerve system 5-12 children rheumatic arteritis neuron cells change proliferation of microglia cells chorea minor

86 Rheumatic pneumonitis and pleuritis uncommon interstitial inflammatory infiltrates fibrous inflammation of the pleural surface hyaline membrane

87 Thanks!