泌尿幻灯课件.ppt

单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,The Diseases of,The Urinary System,Yin Hongling,Department of Pathology,Xiangya Medical College,CSU,Contents,：,Glomerulonephritis,;,GN,Pyelonephritis,Tumor of kidney and bladder,Primary,glomerulonephritis,.,Review,Nephron,Glomerulus,Glomus,Filtering membrane,Mesangium,Bowmans capsule,Renal tubule,Gross,Cortex,Medulla,Pelvis,renal tubule,glomus,Bowmans capsule,electron microscope,.,Pathogenesis,It is a kind of,allergy,disease that mainly,damage,glomerulus.,Classification:,Primary,Secondary,Injury courses,：,First,：,Immune complex is located in the,glomerular,two patterns,Second:,Glomerular injury,How?,1.,In situ immune complex deposition,Antibodies react,directly,with fixed,or planted antigens in the glomerulus.,Anti-GBM nephritis,Heymann nephritis,Antibodies may also react in situ with,antigens of,planted,Antigen,Antibody,Basement membrane deposit,In situ immune complex deposition,Anti-GBM nephritis,：,linear,pattern,2.,Circulating immune complex deposition,Antibody reacts with non-glomerular,ectogenous or endogenous antigens,then IC deposits in glomerular in the process of blood circulation.,Mesangium,Subendothelial,Subepithelial,GBM,IC deposition,Circulating complex,Subepithelial,deposits,Subendothelial,deposits,Circulating immune complex deposition,EM,:,Immune complex is also called,electron dense deposits,granular pattern,3.The antibodies of Anti-glomerular cells,4.Cellular immunity,5.The activation of complement,6.The mediators of glomerular injury,IC,沉积于滤过膜上,中性粒、单核细胞,浸润,蛋白酶、氧自由基、花生四烯酸、细胞因子：,IL-1,TNF,GBM,受损通透性升高,蛋白尿、血尿,系膜细胞增生及基质硬化,C5a,C5bC9,系膜细胞,PDGF,TGF-,Complement neutrophil-mediated mechanism,.Pathologic diagnosis,Renal needle biopsy,LM,：,HE Staining.Special Staining,：,PAS PASM Masson,Immunofluorescence,：,IgG,、,IgM,、,IgA,、,C,3,EM,.Basic pathological changes,1.肾小球细胞增多,2.基底膜增厚和系膜基质增多,3.炎性渗出和坏死,4.玻变、硬化,HE Staining,：,normal glomerulus,hypercellularity,Proliferous epithelial cells,GBM become thick,GBM become thick,GBM become thick,PAS staining,：,proliferation,of mesangial matrix,Neutrophil exudation,Hyalinization&,sclerosis,.Clinical patterns,1.,急性肾炎综合征,Acute nephritic syndrome,2.,快速进行性肾炎综合征,Rapidly progressive,nephritic syndrome,3.,肾病综合征:,nephrotic syndrome,NS,三高一低,:,高,蛋白尿、,高,度水肿、,高,脂血症、低蛋白血症.,肾,炎,滤过膜通透性,高度蛋白尿,3.5g/24hr,低蛋白血症,30g/L,血浆胶体渗透压,组织间液,高度水肿,肝脏合成脂蛋白,高脂血症,4.,无症状性血尿或蛋白尿,Asymptomatic,hematuria,or proteinuria,5.,慢性肾炎综合征,Chronic nephritic syndrome,6.,尿毒症,Uremia,尿改变,尿量,尿质,少尿、无尿,多尿、夜尿,血尿,蛋白尿,管型尿,水肿、高血压,氮质血症,尿毒症,.Classification,Acute diffuse proliferative GN,Rapidly progressive GN,Membranous GN,Minimal change disease,MCD,Focal segmental glomerulosclerosis,FSGS,Membranoproliferative GN,Mesangial proliferative GN,IgA nephropathy,Chronic GN,（一）急性弥漫性增生性肾炎,Acute diffuse proliferative GN,Postinfectious GN,1.,病因、发病机制,最常见的病原体是：,A,族乙型溶血性链球菌中致肾炎菌株（,12,、,4,和,1,型）,HE Staining,：,normal glomerulus,Neutrophile exudation,hypercellular,proliferative endothelial&mesangial cells,Cellular swelling,Hump,Hump,Hump,IgG-ir,red cell cast,Protein cast,2.,病变,（,1,）大体：,大红肾,red large kidney,、,蚤咬肾,（,2,）光镜：,内皮细胞和系膜细胞增生,（,3,）免疫荧光,:,颗粒状荧光,IgG,、,C,3,沉积,（,4,）电镜：增生,+,上皮下电子致密沉积物,（驼峰状,“,hump,”）,3.,临床病理联系,Acute nephritic syndrome,（,1,）（,2,）（,3,）,（二）、快速进行性肾小球肾炎,Rapidly progressive GN,RPGN,Extra-capillary GN,1,、病理变化,:,（,1,）光镜：概念：,新月体,(Crescent),?,分为几个阶段,?,如何形成,？,对肾功能有何影响,?,诊断,?,新月体形成的肾小球数,50%,新月体的体积,50%.,（,2,）电镜：,GBM,严重受损,：断裂、缺损。,2,、临床表现：,Rapidly progressive nephritic,syndrome,新月体,(Crescent),:,由增生的壁层上皮细胞、单核细胞和炎症细胞构成,附着在,肾球囊层，在血管球外侧,形成新月形或环状结构。,Cellular,Crescen,t,Cellular,Crescen,t,Cellular,Crescen,t,Fibrous-cellular,Crescen,t,Fibrous-,Crescen,t,Fibrinogen,-,ir,3,、病因、分类,型,RPGN,：,抗肾小球基底膜性肾炎。,肺出血肾炎综合征,Goodpasture syndrome,抗,GBM,抗体与肺泡基底膜交叉反应，咯血、,血尿、蛋白尿、轻度高血压、肾衰。,型,RPGN,：,免疫复合物性肾炎。,型,RPGN,：,原因,不明，血管炎，较多见。,Goodpasture syndrome,IgG-ir,（三）引起,肾病综合征,的肾炎类型,膜性肾小球肾炎,Membranous GN,为,慢性免疫复合物性肾炎，原发性,为自身免疫性疾病即自身抗体与肾小球上皮细胞膜抗原反应，形成上皮下沉积物；继,发性,为,免疫复合物沉积,，,如：乙肝肾，,SLE,等。,膜攻击复合体,C5b-C9,激活系膜细胞,蛋白酶、氧化剂，可在无中性粒细胞参与时引起肾小球损伤。,Capillary walls are,thickened,spikes,electron,dens deposits,Spikes,Silver staining:spikes,spikes,(1)光镜:,弥漫性毛细血管壁（基底膜）增厚,细胞不增生无炎症细胞浸润，按病程分四期。,(2),大体,:,大白肾,(3),荧光：,颗粒荧光、,IgG,、,C,3,沉积,(4),电镜：,上皮下电子沉积物、钉突形成,(5),银染：,钉突（,spikes,）、梳齿,(6),临床：,见于成人，病程长，主要表现为,肾病综合征,，,激素治疗不敏感，,25%,患者发展为肾衰。,轻微病变性肾炎,Minimal change GN,Lipoid,nephrosis,（,1,）病变特点：,光镜：肾小球正常，,近曲小管上皮细胞内出,大量脂滴和玻璃样小滴,；肉眼：肾切面上见黄色条纹；荧光和电镜：无沉积物，弥漫性,脏层上皮细胞足突消失。,Foot processes disappear,Foot processes disappear,（,2,）临床,:,肾病综合征,(,选择性蛋白尿,）激素治疗敏感,预后好,.,（,3,）机制,:T,（,Th2,细胞占优势）细胞功能紊乱密切相关，细胞因子样物质，滤过膜阴离子,3,、,局灶性节段性肾小球硬化,Focal segmental glomerulosclerosis,FSGS,（,1,）光镜：,局灶性、节段性,分布，系膜基质增,多、基底膜塌陷、玻璃样物沉积、肾小球硬化,。,（,2,）电镜：系膜基质增多，,上皮细胞足突消失。,（,3,）,荧光：,IgM,、补体沉积,（,4,）临床：为肾病综合征，半数,10,年内发展为,肾衰，预后差。,Segmental sclerosis,FSGS:collagen deposition(blue),FSGS:IgM-ir,SGS,（,1,）光镜：,系膜细胞及基质增生，系膜区增宽，管壁增厚，分叶状结构更明显。,4,、膜性增生性肾炎,Membranoproliferative GN,MPGN,系膜,插入,A mesangial cell is interposing between the endothelial cell and basement membrane,PAS staining:double-track,MPGN type I,Subendothelial,MPGN type II,（,2,）银染或,PAS,染：,系膜细胞及基质,插入,内皮细胞和基底膜之间,使呈管壁,“双轨征”,（,3,）电镜：,型：内皮下沉积,。,型：基底膜内。,（,4,）临床：,血清,C,3,降低，表现为肾病综合症，,少数为血尿和蛋白尿，病变重，进,展快，,50%,病例在,10,年内出现肾衰,（,1,）光镜：,系膜细胞增生伴基质增多，系膜区增宽，,但管壁不增厚。,5.,系膜增生性肾炎,Mesangial proliferative GN,（,2,）电镜：,系膜增生,+,电子致密物沉积。,（,3,）荧光：,IgG,、,IgM,、,IgA,、,C,3,沉积。,（,4,）临床：,青年好发，以无症状性血尿和蛋,白尿为主，少数为肾病综合征，一,般预后好，,2-3,年内好转，少数发,展为慢性。,三种带,膜字,肾炎的区别：,膜性,肾小球肾炎；,膜,指基底膜增厚。,膜性,增生性肾小球肾炎：,膜,指系膜增生,和,基底膜增厚,。,系膜,增生性肾小球肾炎：,膜,仅指系膜增生,（四）,IgA,肾病,IgA nephropathy,，,BergerDisease,全球最常见的肾炎类型，我国大约占,30%,；,机制不明，呼吸道炎症时，粘膜,IgA,合成增加并,在系膜区沉着,。,临床：,复发性肉眼血尿为主，蛋白尿轻。,少数,为肾病综合征，多见于儿童和青年。,IgA-ir,荧光：,系膜区单纯性,IgA,（,+,）沉积，,为本病的特征及诊断依据。,Proliferative mesangial and matrix,光镜：,组织学改变显多样性，以系膜增生,性病变最常见。,（五）、慢性肾小球肾炎,Chronic GN,，,End-stage kidney,不是一种独立的疾病，通常由不同类,型的肾炎发展而来，部分患者起病隐匿，,发现时已是晚期阶段。,（,1,）大体：,继发性颗粒性固缩肾,Secondary granulo-Contracted kidney,（,2,）光镜：,a,、,大部分（,75%,以上）肾小球玻变（玻璃球）和硬化，呈“集中趋势”，所属肾小管萎缩；,b,、病变轻的肾小球代偿性肥大，所属肾小管扩张，有管型；,c,、间质纤维增生和小动脉硬化。,1,、病变：,大体：,继发性颗粒性固缩肾：,变形、变小、变轻、变硬、变薄、变浅。,与原发性颗粒性固缩肾如何区别？,sclerosis,Masson staining,：,sclerosis,Compensatory hypertrophy,Tubules are often dilated and filled with pink casts,The artery walls are thickened,2,、临床,：,慢性肾炎综合征：多尿、夜尿和低比重尿，有时伴蛋白尿和血尿；肾性高血压；贫血；氮质血症、尿毒症伴全身中毒症状。,预后差，死于尿毒症、心力衰竭、脑溢血或继发感染。,We can see three kidneys from this picture,Why?,透析,4,年患者的肾脏,2,、病因和发病机制：,肾盂肾炎,pyelonephritis,1,、概述：,肾盂肾炎是感染引起的累及,肾,盂、肾小管和肾间质,的,化脓性,炎症；,分为急性和慢性两种；,女性多见.,（一）、急性肾盂肾炎Acute pyelonephritis,gross,：,Micro-abscess,切面：髓质内见黄色条纹，向皮质延伸。,white cell cast,1,、大体：,有脓肿形成,2,、光镜：,肾盂、间质性化脓性炎症、脓肿形,成伴肾小管坏,死，肾小球很少受累。,3,、并发症：,急性坏死性乳头炎、肾盂积脓、,肾周围脓肿。,4,、,临床病理联系,：,全身症状、膀胱刺激症,状，尿液检查：脓尿、蛋白尿、管型尿、菌尿、,血尿，,白细胞管型,有诊断意义。,Anomalous,scar,1,、大体：,表面：,双肾病变不对称：,体积变小、质地变硬、表面变形：,不规则凹陷性疤痕为特征,。,（二）、慢性肾盂肾炎,Chronic pyelonephritis,切面：,皮质变薄；肾乳头萎缩；肾盂肾盏变形；肾盂黏膜粗糙，颗粒状。,Chronic glomerulonephritis,Chronic pyelonephritis,2,、光镜：,肾盂粘膜、肾间质,慢性化脓性,炎症；,肾小管萎缩、坏死，有管型；,肾球囊周围纤维化,，,最终肾小球硬化；,小动脉玻变及硬化。,3,、临床病理联系：,常急性发作；肾小管功能受损,多尿、夜尿，电解质紊乱；,X,线肾盂静脉造影,肾盂肾盏变形，肾脏体积缩小；,肾性高血压；晚期出现肾衰。,与慢性肾小球肾炎何区别：,病因、机制、炎,症性质、病变特点（肉眼、镜下）、临床表,现和结局。,Tumor of kidney and bladder,Renal cell carcinoma,Gross,LM,clear cell carcinoma,papillary carcinoma,chromophobe renal carcinoma,Clinical course,：,hematuria,、,flank pain,、,palpable mass,The renal cell carcinoma that on sectioning is mainly cystic with extensive hemorrhage,Clear cell carcinoma,clear cell,carcinoma,Capillary,Granular pink cytoplasm,papillary,carcinoma,Nephroblastoma,This is Wilms tumor,：,this small kidney from a 4 year old child contains a lobulated tan-white mass.,Clinical course:,Hematuria and,palpable mass,Primary glomerular and tubular structures,Primary tubular structures,Striated,muscle differentiation,Transitional cell carcinoma of the,urinary bladder,部位,大体：,息肉样、乳头状、菜花状和溃疡状。,镜下：,根据是否有乳头状结构、细胞层次、,异,型性、浸润深度，将移行细胞分为：,O,、,、和级。,临床：,血尿、膀胱刺激症状、肾盂积水和肾盂肾,炎。,Transitional cell carcinoma,grade,0,Transitional cell carcinoma grade,Homework:,Concepts,：,crescent,nephrotic syndrome,red,large kidney,Secondary granule Contracted kidney,.,Questions,:,1、试述急性弥漫性增生性肾小球肾炎的主要病变,及临床病理联系。,2、试述快速进行性肾小球肾炎的主要病变及临床,病理联系。,3、试比较慢性肾盂肾炎与慢性肾炎的异同。,4、引起肾病综合征的肾小球肾炎有哪些？,5、在泌尿系统疾病中可能出现血尿的疾病,有哪些？,6、有系膜细胞增生的肾小球肾炎有哪些？,7、一病人,7岁时有过水肿，少尿、血尿、蛋,白尿的病史,以后多次发作，45岁时出现,多尿、夜尿、头昏、贫血、肾衰，试分析,患者先后患何病？写出诊断及主要依据。,THANKS,