泌尿系統(tǒng)疾病英文

1、泌尿系統(tǒng)疾病英文Section 1 Introduction A. Anatomy of kidney Cut surface of kidney Cortex Medullary Renal papilla Calyx Renal pelvis B. Histology of kidney Nephrons: capillary tuftGlomerulus bowmans capsule (capsular Space) proximal convoluted tubulerenal tubules distal convoluted tubule C. Ultrastructure of

2、 glomerulus 1. Glomerular filtration barrier:basement membrane (B. M)endothelial cell Visceral epithelial cell (podocyte), foot-process have plenty negative ion substances (heparan etc) 2. Glomerular mesangium structure mesangial cell mesangial matrix ,D. Classification of urinary system disease 1.

3、Glomerulonephritis 2. Pyelonephritis 3. Tumor of kidney 4. Tumor of bladder D. Classification of Glomerulonephritis primary Glomerulonephritis (1) glomerular minor 1esion (2) focal and segmental glomerular change A. focalnephritis B. focal and segmental glomerulosclerosis (3)diffuse glomerulonephrit

4、is A.membranous glomerulonephritis (membranous nephropathy) B. proliferative glomerulonephritis a. mesangial proliferative glomerulonephritis b.endocapillaryproliferative glomerulonephritis c. mesangiocapillary glomerulonephritis (membranoproliferative glomerulonephritis type I and III) d. crescenti

5、c glomerulonephritis e. IgA nephropathy C. sclerosing glomerulonephritis (4)unclassified glomerulonephritis secondary Glomerulonephritis (1)1upus nephritis (2) nephritis of Henoch-Schonlein purpura (3) anti-GBM nephritis, Goodpasture syndromeSection 2 Glomerulonephritis (GN) A. Definition Glomerulon

6、ephritis is a hypersensitivity inflammatory disease. It cause by various immune complex and appear diffuse glomeruli proliferative inflammation in bilateral kidneys shortened form B. Mechanisms of glomerular damageIt is clear that GN can be readily induced by antigen-antibody reactions.1. Antigens E

7、ndogenous antigen (intrinsic) GBM, endothelial cell, mesangial cell Exogenous antigen (incoming) bacteria, virus, fungus, parasit, drug ect 2. Immune injury mechanismsimmune complexs formed In situ (10%) (immune complex nephritis in situ) Antibodies react directly with, intrinsic tissue antigen (GBM

8、,EC,MC ) or antigen planted (non-glomerular antigen) YY YYYYYYYYGBM-autoantigenimmune complexs formed In situ Immunofluorescent (IF) appear linear pattern:Green color linear fluorescencefibrin (2) Circulating immune complexs deposition (90%) The antigen and antibody have not immunologic specificity

9、for glomerular constituents, antigen-antibody complexs are formed in the circulation and then deposit in the glomeruli. IF appear granular pattern. Simulative picture of capillary tuft IF appear granular pattern. Immune complexComplement activated mononuclear cell activated plateletMCcytokinesC5-9C3

10、,C5aneutrophilInjury of glomeruliReleasing proleasefree radicalsarachidonic acidExudation, proliferative inflammationC. Common glomerulonephritis . Acute diffuse proliferative GN called also:endocapillary proliferative GN,endothelial-mesangial proliferative glomerulonephritispost-streptococcus GN De

11、finitionMC and EC mainly /diffusely proliferation in most of glomeruli in both kidneys.Its abnormal reactive inflammation or proliferative inflammation. Frequently in children EtiologyAssociated with A-haemolytic streptococcal (type 12,4,1) infection. Within 1-4 weeks after infection, not at that ti

12、me.Other organisms: pneumococci, viruses, Malaria etc. ,Morphology Grossly: “big and red kidney “flea-bitten kidney Enlargement,tight capsula,Dark-red colourbleeding pointparasite parasite LM: 1. glomeruli: a. proliferativ alteration: All the glomeruli are enlarge, and filled with cells (mesangial a

13、nd endothelia cell), capillary lumen narrowed. But parietal epithelium without hyperplasia b. Exudative alteration: variable infiltration of polymorphonuclear leukocytes, RBC in capillary tuft and Bowmans capsule. c. thrombosis and fibrinoid necrosis of capillary tuft, bleeding .2.Renal tubules alte

14、ration: degeneration of epithelial cells, red cell and leukocyte casts etc.3.Interstitial alteration: congestion, edema, inflammatory cell infiltratingneutrophilsBiopsy of aspiration in kidney glomerule enlarge, and filled with cells (mesangial and endothelia cell), capillary lumen narrowed. parieta

15、l epithelium without hyperplasianeutrophilssilver stainingGBM, Mesangial dark colourMasson stainingout GBM, Eosin-protein deposite EM and IF: endothelial cell and mesangial cell proliferating, in the basement membrane and under the podocyte have hump-shaped deposite. IF appear granular pattern- IgG.

16、 C3 (+)IF appear granular patternhump-shaped deposite.Camel peak-like Clinical-pathological correlation Acute nephritis syndrome Urine alteraion: Oliguria (lower than 400 ml/24h) or anuria (lower than 100 ml/24h) Proteinuria, cast (+) Hematuria Edema (sodium, water retention) Hypertension (blood vol

17、ume) heart failure hypertensive encephalopathy Glomerule filtration azotemia renal failurediuretic agentmilliliter Remove, save up ,Result : 95% would be cured, 5% might turn to chronic GN, and few cases develop rapidly progressive GN. femalecause of death: pulmonary hemorrhage, renal failure, Diffu

18、se membranous GN membranous nephritis) Early chronic nephritis, the duration is slow and prognosis is relatively good 1. Pathology (1) LM: basement membrane diffusely thickened very much (platinic ring-like), but the capillary lumen is not obstructed usually. No cell proliferation. (2) grossly: “big

19、 and white kidney.(3) EM: There are “dome and “spike. Dome is the deposit, spike is the proliferation of “basement membrane substance . So the BM becomes thickened and late stage BM becomes “moth-eaten like. (4)IF: granular pattern- IgG.C3 (+)“spike“dome“moth-eaten likethe proliferation of “basement

20、 membrane substanceimmune complex depositMasson stainingout GBM, Eosin-protein deposite 2. Clinical-pathological correlationTypical nephrotic syndrome High proteinuria (osmotic pressure of filtration barrier increase ) High edema (proteins losecolloid-osmosis pressuredecrease) High cholesterolemia a

21、nd lipidemia Low blood albumin (proteins lose),highhighhighlow3. Result The duration is slow. Most of cases develop recurrent, in late stage a number of glomeruli develop fibrosis, some cases may be cure. Diffuse membranous proliferative GN mesangiocapillary GN) It is a chronic progressive nephritis

22、 and it affects the mesangium and capillary of glomerulus. It is more serious than membranous nephritis. Its prognosis is worse, easier to transit to atrophic kidney. 1. Pathology LM: The glomerulus becomes lobulatedcapillary wall thickened and lumen narrowedSome hyaline glomeruli would be seen. (2)

23、 EM: Mesangial cell and mesangial matrix proliferate very much further more, they would insert into the capillary wall, the BM show splitting (two layer). Making the lumen seriouly narrow, the immune deposit can be seen elsewhere (mesangium and capillary wall). (3)IF: granular pattern- IgG.C3 (+) -M

24、esangium, capillary wall deposit. Mesangial cell and mesangial matrix proliferate very much and insert into the capillary wall, the BM show splitting (two layer).Railway-like 2. Clinical-pathological correlation The early stage: proteinuria and hematuria is mild degree. The disorder affect BM: nephr

25、otic syndrome The late stage: hypertension and renal failure. 3. Result The prognosis is worse easier to transit to atrophic kidney, the 50% of cases develop chronic renal failure within 10 years. . Minimal change glomerulonephritis Lipoid nephrosis)1. Pathology:(1) Glossly: big and white kidney (2)

26、 LM: glomeruli no change at all tubules: fatty degeneration.(3) EM: The unique change under EM is foot processes fusion. No deposit at all. big and white kidney2. Clinical-pathological correlation Nephrotic syndrome (three-high and one-low)(1) High proteinuria (mainly is albumin)(2) Hypoalbuminemia

27、(3) High edema (4) Hyperlipidemia and hypercholesterolemia highhighhighlowInjory of glomerular capillary wallFiltration of albuminGenerous proteinuriaplasma proteinHypoalbuminemiaplasma colloid osmotic pressure Water into tissueedemablood volume glomerular filtration rate Aldosterone and antidiureti

28、c hormone Sodium and water retentionaggravatingHigh proteinuriaHypoalbuminemiaHigh edemaHyperlipidemia and hypercholesterolemiaindefiniteHypoalbuminemiaLipoproteins synthesis in liverdisorders of lipid granule transportation in blood and breakdown of peripheral lipid proteins 3. Result The prognosis

29、 is good 90% of cases in children would be cure with cortisone . Diffuse sclerosing GN Chronic nephritis) This type is the final result of a lot of GN (end-stage kidney), its character is majority of nephrons (glomeruli) become hyalinized, fibrosis, so uremia, even. renal failurePathologic character

30、:majority of nephrons (glomeruli) become hyalinized, fibrosis Residual nephrons become compensative hypertrophyGrossly “granular atrophy of kidney causes:1.Morphology:(1) grossly: granular atrophy of kidney Granule collecting areas of compensative hypertrophy nephronsDepressed- collecting areas of f

31、ibrosis of nephrons(2) LM:Most of glomeruli are partially or completely scarred and some converted to hyaline masses the nearby tubules are atrophy and fibrosis;Fibrosis of interstitial tissue is prominent, and there is an inflammatory infiltration in stroma Relatively normal glomeruli occur compens

32、ation, glomeruli occur hypertrophy and tubules dilate Fobrosis and hyelinzed of glomeruliatrophy and fibrosis of tubulescompensative hypertrophy of nephron and tubules dilatean inflammatory infiltration in stroma 2. Clinical-pathological correlation Chronic nephritis syndrome (1) Renal failure: azot

33、emia uremia (2) Hypertension(3) Proteinurea and edema are not severe (4) Polyuria and nocturia renin3. Result Prognosis is very bad, the death causes are: (1) uremia(2) Hypertensional heart disease and cerebral hemorrhage (3) Infection VII IgA NephropathyIgA Nephropathy (Berger Disease): is the most

34、 common glomerular disease.Presence of prominent IgA deposits in the mesangial regions. Dx by immunocytochemical techniques.Frequent cause of recurrent gross or microscopic hematuria, nephrotic syndrome may be present.Affect children and young adults,.Associated with gluten enteropathy, liver diseas

35、e. IgA depositionVIII Focal Segmental Glomerulosclerosis (FSG):Sclerosis of some glomeruli; portions of capillary involved. Clinically show nephrotic syndrome or heavy proteinuria. Idiopathic responds poorly to steroids and progress to chronic renal failure. Causes: associated with HIV, drug abuse,

36、sickle cell disease, IgA nephropathy, certain inherited disease and as primary disease, idiopathic. Sclerosis of some glomeruli; portions of capillary involved.Section 3 Pyelonephritis A. Definition: Pyelonephritis is a suppurative inflammation of renal pelvis, renal stroma and renal tubes, it is ca

37、used by pyogenic bacteric infection directly Not irritability B. Etiology and pathogenesis . Etiology: colon bacilli (60-80%) proteus staphylococci etc Ages:child-bearing age females and infants frequently, female:male=910:1 In clinic: high fever, aching pain in the waist, hematuria, pyuria. irritat

38、ion sign of bladder: urinary frequency, urgency, urodynia. uremia renal failureratio,. Infective path1. Ascending infection: (urethra infection, main path) urethrabladder ureter renal pelvis renal stroma and renal tubules (glimerulus not affected). Organism: colon bacilli, women affect more easily o

39、ne side kidney affected frequently. 2. Descending infection: (hematogenous infection) seldom. primary focusblood stream kidney cortex renal stroma and renal tubules renal pelvis (glimerulus affected). organism: staphylococci, double kidneys affected frequently. The role of urinary tract obstructiong

40、ravidity uterus ureter compressed urine retentionurinary stone urinary tract obstructionprostate hyperplasia Defensive function of urinary tract (IgA , WBC , clearance role of urine flow )bacteria grow in the urine (culture medium),C. Pathological type . Acute pyelonephritis 1.Definition: acute supp

41、urative inflammation of pelvis, renal stroma and renal tubules.2. LM: renal stroma and pelvis develop suppurative inflammation, forming abscess mainly, tubules filled with liquor pus . Ascending infection: pelvis and renal stroma predominance Descending infection: glomeruli and renal tubule around f

42、irst affect renal stroma develop suppurative inflammation, tubules filled with liquor pus . renal stroma develop suppurative inflammation, forming abscess, tubules filled with liquor pus . 3. Grossly: The kidney is enlarge, surface show size and shape irregular abscesses, some abscesses are long sha

43、ped according to the “medulla radiate streak structure, pelvis hyperemia and even purulent exudate covered. Acute pyelonephritis: size and shape irregular abscesseson surfaceAcute pyelonephritis Abscesses size and shape irregular abscesseson surfacesome abscesses are long shaped according to the “me

44、dulla radiate streak structure4. Clinical-pathological correlation(1) Infective symptom: high fever, aching pain in the waist, (2) irritation sign of bladder: urinary frequency, urgency, urodynuria. (3) pyuria, proteinuria, hematuria, casts in urine, 5. Results : The most of cases would be cure, but

45、 when its treatment is uncomely, it may be recurrence and turn to chronic pyelonephritis. Chronic pyelonephritis 1. Definition: chronic suppurative inflammation of pelvis, renal stroma and renal tubules.2. Causes: Acute pyelonephritis would transit to chronic the cause may be as follows: Treatment n

46、ot thorough enough Bacteria metamorphosis (become L- type )Urinary tract obstruction 3. Grossly: Irregular scars scattered at the kidney. Cortex become thin, pelvis and calices are dilated, the mucosa is coarse “Large scar concave atrophy of the kidney Cortex become thin, pelvis is dilated, the muco

47、sa is coarse “Large scar concave atrophy of the kidney 4. LM: (1) Chronic purulent inflammation, fibrosis (2) Renal parenchyma destruction: hyalinized glomeruli and atrophic tubules are evident but some dilated tubules have big cast inside (thyroid tissue like ) Cortex become thin, pelvis is dilated

48、, the mucosa is coarse “Large scar concave atrophy of the kidney some dilated tubules have big casts inside (thyroid tissue like ) some dilated tubules have big casts inside (thyroid tissue like ) Proliferation of transitional epithelium 5. Clinical-pathological correlation The symptoms are not mark

49、ed (1) Urorrhagia ( Polyuria)(2) Neutrophils in urine will add (3) Urine culture bacteria will (+)(4) final, hypertension and renal failure 6. Result: The prognosis is poor. Most of cases die. dead causes:(1) Renal failure, urinemia (2) Hypertensive heart disease and hypertensive brain disease Secti

50、on 4 Renal carcinoma (renal cell carcinoma, clear cell carcinoma )A. Definition: Renal carcinoma is a malignant tumor, it is originate from renal tubule epithelium. 80-90% of renal malignant tumors. 60 ages，malefemale = 2:1occupy B. Mophologic changes. Grossly: Nodular, might have a pseudocapsula, u

51、sually on the upper pole of the kidney; yellow colored, hemorrhagic and necrotic (“five-color kidney) Nodular, a pseudo capsula, on the upper pole of the kidney; yellow colored, hemorrhagic and necrotic Nodular, a pseudo capsula, on the upper pole of the kidney; yellow colored, hemorrhagic and necro

52、tic Soft, calcify . LM: The cancer cells are clear (lipid and glycogen deposition), nuclei not big, nucleus-cytoplasm ratio not large. Cancer cells arrange nest-like or gland-like. Stroma is scanty. cancer cells are clear, nuclei not big, nucleus-cytoplasm ratio not large, arrange nest-like or gland

53、-like. Stroma is scanty. cancer cells are clear, nuclei not big, arrange nest-like or gland-like. Stroma is scanty. C. Spread of tumor and clinical features . Hematogenic metastasis: early stage , lung, bone, liver, adrenal gland, brain. Peculiar site: nose, mouth, throat, vagina, eye Retrograde met

54、astasis: left kidney tumor left renal vein left spermatocord vein left epididymis ,. Hematuria without pain . Atopic endocrine syndrome (para-tumor syndrome) e.g. parathyroid hormone, renin, gonad stimulating hormone, adrenal cortex (ACH) hormone, erythropoietin (EPO).D. Results The prognosis is poor No operation: die within 1 year Operation: 2 years survival 67% 5 years survival 50% 10 years survival 34%Section 5 Nephroblastoma (embryonal adenosarcoma, wilms tumor)A. Definition : Nephroblastoma is a maligna