《医学ppt课件：英文肾小球疾病.ppt》由会员分享，可在线阅读，更多相关《医学ppt课件：英文肾小球疾病.ppt（57页珍藏版）》请在三一办公上搜索。
1、Chapter 2 Outline of Renal Glomerular Diseases,Definition Glomerular Diseases are characterized by a group of similar clinical manifestations,such as hematuria,proteinuria,hypertension,but their etiology,pathogenesis,pathology and prognosis are different,involving bilateral glomerulus changes,Classi
2、fication,PrimarySecondaryHeredity,Classification of primary glomerular diseases:1.Clinical types:acute glomerulonephritisrapidly progressive glomerulonephritischronic glomerulonephritislatent glomerulonephritis nephrotic syndrome,2.Pathological types:minimal glomerular abnormalitiesfocal segmental l
3、esionsdiffuse glomerulonephritismembranous nephropathy,proliferative glomerulonephritis:mesangial proliferative glomerulonephritisendocapillary proliferative glomerulonephritismesangiocapillary glomerulonephritiscrescentic&necrotizing glomerulonephritissclerosing glomerulonephritis unclassified glom
4、erulonephritis,minimal glomerular,focal segmental lesions,membranous,Mesangiocapillary,Mesangial proliferative,Endocapillary proliferative,crescentic,necrotizing,Sclerosing,Most of the glomerulonephritis are immune mediated inflammatory disease,however the reaction is a primary cause for the glomeru
5、lonephritis.Inflammatory mediators(such as complement,interleukin),taking part in immune reaction,results in glomerular injury and clinical symptoms.In the chronic development of glomerular disease,it can also be due to non-immune and non-inflammatory mechanisms,Pathogenesis:,1.Immunoreaction:humora
6、l immunity：circulatory immune complex(CIC)immune complex format in situs autoantibody cellular immunity：important for some types;,circulatory immune complex(CIC),immune complex format in situs,2.Phlogistic reaction:Inflammatory cell monocyte macrophages,neutrocytes,acidophils&platelet Mediators of i
7、nflammation complement,leukotriene,etc.3.Non-immunologic mechanism:important factors of diseases persistence&deterioration large amount of proteinuria,hyperlipemia,loss of body fluid,etc,Clinical manifestation:1.proteinuria:positive150mg/d;large amount of proteinuria3.5/d;protein of molecular weight
8、24104 can pass normal renal filter membrance(lysozyme,2microglobulin,light chain protein)protein in normal urine150mg/d(TatomHorsfall pro.&urethral tissue pro),only about 30mg/d of albumin.,Both charge and size selectivity normally can prevent virtually all of plasma albumin globulin and other large
9、-molecular-weight protein from crossing the glomerular wall.If the barriers are disrupted,there can be leakage of plasma proteins into the urine.,电荷屏障：1上皮细胞 2基底膜 3内皮细胞 4被滤过物质,2.hematuria:RBC3/HP of centrifuged hematuria microscopic hematuria;blood1ml/l urine gross hematuria;painless&whole hematuria,
10、RBC casts,protein excretion500mg/d may glomerulus originated hematuria,distinguish the origin of hematuria:fresh urine sediment test under phase contrast microscope distortion RBC hematuria indicate glomerular originatedreason:GBM rupture,when RBCs passing,they will be pressed to distortion.Irregula
11、r shapes of RBCs may also occur due to PH and osmolarity changes found in the distal tubule.distribution curve of urine RBC volume,Isomorphic red blood cells in urine,a,b,c,d,3.edema:nephropathy:hypoproteinemia clinically heavy proteinuria hypoalbuminemia and diminished colloid osmotic pressure prom
12、otes a net movement of fluid into interstitium hypovolia and initiates the edema-forming sequence.,nephritis GFR retention of sodium and water;begin from eyelids;Be local and evident in the very soft tissues of the eyelids/face and tends to be most pronounced in the morning.the increased capillary p
13、ermeability GRF.,4.hypertention:90%of CKD patients gets HBp persistent deterioration of renal function mechanism:retention of sodium and waterrenin excretedecompressing materials in kidney(prostate,kinin)5.Renal function damage,Chapter 3 Primary Glomerular Diseases,Definition AGN:The acute nephritic
14、 syndrome is the clinical correlate of acute glomerular inflammation.In its most dramatic form,the acute nephritic syndrome is characterized by sudden onset of azotemia、edema、hyertension、hematuria and proteinuria.,Section 1.Acute Glomerulonephritis AGN,【Pathogeny&pathogenesis】Pathogeny hemolytic str
15、eptococcus infection(upper respiratory tract infection),pathogenesis CIC accumulate in glomeruli/immune complex in situ activate complements endothelial cells&mesangial cells regeneration and soakage of neutrocytes&monocytes renal pathological changes.,【Pathology】Endocapillary proliferative glomerul
16、onephritis endothelial&mesangial cellsCrescents are uncommon.Immunofluorescence microscopy reveals diffuse granular deposition of IgG and C3 in subendothelial and mesangial areas.The characteristic finding on election microscopy is the presence of large electron-dense immune deposits in the subepith
17、elial areas.,Endocapillary proliferative,Normal glomerulus,【Clinical manifestation,【Clinical manifestation&Lab.Exam】,3.Edema;typical eyelid4.HBp:water&sodium retention 5.olyguria(400ml/d),moderate azotemia.mild acute renal failure6.heart failure:water&sodium retention and hypertension 7.C3 decrease
18、but restore in 8 weeks,serumal ASO may increase8.Generalized symptoms:anorexia,nausea,vomiting,malaise.Swelling of the renal capsule can cause flank or back pain.,【diagnosis hematuria earlier,【diagnosis&deferential diagnosis】,2.RPGN:rapidly deteriorate renal failure3.Systematic disease:SLE or purpur
19、a4.Indication of renal biopsy:olyguria for more than 1 week or gradually olyguria companied by azotemia course continue beyond 2 months AGN companied by nephrotic syndrome,【treatment】,1.Rest until the symptom alleviated;salt,water and protein should be limited.2.Antibiotics penicillin 1014days3.Diur
20、etics and antihypertensive agents are employed to control extracellular fluid volume and blood pressure;4.Dialyze short time;5.Chinese herb,【prognosis】,1.symptoms,signs&lab exam recover in 48 weeks2.1%die for acute renal failure3.6%18%shift to chronic glomerulonephritis,Section 2.Rapidly Progressive
21、 Glomerulonephritis(RPGN)Gist:1.pathology:crescent glomerulonephritis;2.rapidly deteriorate of renal failure is the character 3.intensified plasma replacement therapy 4.methylprednisolone impaction accompanied with CTX therapy monly turn into chronic nephritis,Crescent of Rapidly progressive glomeru
22、lonephritis,Section 3.chronic glomerulonephritis Hematuria,proteinuria,edema【pathology】Diffused glomeruli sclerosis in late stage,慢性肾小球肾炎,病理,肾小球纤维化，肾小管萎缩，肾间质炎症细胞浸润,sclerosing glomerulonephritis,【manifestation】1.Symptoms of nephritis dormant,atypical 2.HBp&its complication especially the retina chang
23、e 3.Acute onset in chronic course(infection,labor,kidney-toxic drug)4.Renal failure,【diagnosis,【diagnosis&deferential diagnosis】,Secondary nephritis:SLE,allergic purpura,etc.Alport syndrome:bland,deafness AGN:C3 dont fluctuation HBp renal damage:renal tube damage such as nocturia,【treatment】1.Goal:n
24、ot eliminate urine abnormality but protect renal function;2.Control HBp actively;reduce the proteinuriaproteinuria1g/d,Bp130/80mmgh ACEI or ARB:according to GBM,they may protect renal function,【treatment】,3.Protein&phosphate should be limited in azotemia4.Persandin or aspirin5.Glucocortical hormone&
25、cellular toxics should be stopped when the curative effect is not contented6.Avoiding deteriorating factors:infection,tire,pregnant&toxic drug,【prognosis】1.Renal failure2.The deciding factor is pathologic type3.Correct protection&treatment are also very important,Section 4.Concealment nephritisGist:1.asymptomatic hematuria(glomerular originated),3.treatment principle:recheck regularly protect renal function excise tonsil Chinese herb,
