【临床医学】丁小强－肾小球疾病

1、肾小球疾病Glomerular Diseases丁小强复旦大学附属中山医院Pathological changes - glomerular injuryClinical manifestations -proteinuria / hematuriaA group of diseases Complicated causes & mechanismsVarious clinical manifestationsDifferent prognosisMultiple treatment primary glomerular diseases secondary glomerular diseas

2、es hereditary glomerular diseases Immune mechanismsHumoral Cell-mediatedNon-immune mechanismsInflammationGlomerular diseasesA. Immune mechanisms (A)deposits of Circulating Immuno-Complex (CIC) circilation antigen+ antibody CIC kidney CIC/deposits antigen extrinsic drugs-nonhomologous serum, penicill

3、in foodsxenogenic protein pathogenspecific serotypes streptococci, HBV, HCV intrinsic nucleusSLE) cytoplasmANCA cellular membrane antigen of tumor antigen of thyroid Why does CIC deposit in the glomeruli?Large area of glomerrular capillaries -more chances to contactNet structure of CIC -easy to depo

4、sit and settle down Clearance dysfunction of mesangial cells, disability of mononuclear macrophage, component or function defect of complements Decrease clearance of CIC (B)in situ Immunocomplex 1. Native renal antigen glomerular basement membrane + anti- glomerular basement membrane antibody (anti-

5、 glomerular basement membrane glomerulonephritis) 2. Antigens trapped or planted DNA+ anti-DNA antibody (Lupus Nephritis)Balance between the deposit and clearance of IC determines the situation of the diseasesPersistence of antigenClearance dysfunction of mesangial cellsdisability of mononuclear mac

6、rophagecomponent or function defect of complements IC deposit clearance B. Cell-mediated immune mechanisms minimal change glomerulopathy ? C. Non immune mechanismsglomerular hypertensionhyperlipidemia (LDL- Cho)advanced glycosylation end products (protein) glomerulosclerosisInflammationMediators of

7、inflammation A group of molecules which act as mediators of inflammation and complicated biological functionOrigin of inflammation mediators in kidneyExtrinsic Cells in kidneyinfiltrative neutrophil, lymphocyte, mononuclear macrophage , platelet Intrinsic cells in kidneyMesangial cells, tubular cell

8、s, endothelial cells Mediators of inflammation - active oxygen and active nitrogen - lipids - complements - cytokines - chemotatic factors - adhesion molecules - growth factors - vasoactive substancesTo arouse or promote - proliferation of cells - accumulation of extracellular matrix - changes of hi

9、stological structure - expression of immunomodulating molecules and adhension molecules Effects of the inflammation mediators Mechanisms of Primary GNimmune non-immune inflammationInflammatory cellsExtrinsic cells Intrinsic cells neutrophil, lymphcyte mesangial cells mononuclear macrophage epithelia

10、l cells platelet, tubular cells endothelial cellsInflammation mediators cytokines TNF,IL-1 growth factors TGF,PDGF chemotatic factors MCP-1,IL-8 complements, vasoactive substances active oxygen and active nitrogenCoagulation and fibrolysis system, enzymeGlomerular injuries Essential in the initiatio

11、nEssential in the progressive periodimmune non-immune initiation end stage Primary GNSites of pathological changesMesangium Mesangial cell Mesangial matrixBasement membranePodocyteFoot processEndothelial cellThe peripheral portion of a glomerular lobulePathological changesLM Mesangial cells, matrix

12、of mesangiumEpithelial cellsEndothelial cellsBasement membraneLoops of glomeruliEM Foot processBasement membraneHyperplasy of mesangium (electron-dense deposits )IF Sites, appearances and types of the deposit (Ig or C) Basical changesProliferationFibrosis and sclerosisNecrosisInfiltration of inflamm

13、atory cellsExtents of Injuries primary GN glomerular injuriesonly or dominating changes secondary GN glomerular injuries a part of systematic diseases diffuse impaired glomeruli50% focal impaired glomeruli 50% segmental impaired capillary loops of a glomerule g/d或50mg/kg/dhematuria RBC 3个/HP (fresh,

14、 10 ml sample, 1500rmp centrifuge for 5 min, sediment observation) gross hematuriaRed color of urine, 1ml blood /1L urine hematuria RBC from glomerulisqueezing through GBM dismorphic RBCPhase-contrastmicroscopydismorphic RBC50 Hypothesis:glomerular bleedingdismorphic RBC70% Final diagnosis:glomerula

15、r bleeding Urinary RBC volume distribution curvedissymmetry curveMCV of urinary RBCthat in bloodchanging when passing tubules with different osmosisedema fluid retention in tissue spaces peripheral edema fluid retention in serous cavity glomerular diseases GFR large amount of urinaryprotein lostIntr

16、insic RAS & Aldosterone hypoalbuminemia water & sodium filtration colloid osmotic pressure water & sodium readsorption primary water & sodium retention secondary water & sodium retention Effective circulation blood volumn edema Effective circulation blood volumn Hypertension glomerular diseasesprima

17、ry water & stimulus, such asischemiasodium retentionVolumn-dependent vessoconstrictive vessodilatory substances substances RAS,Ald PGI2,PGE2 vessoactive substances-dependent Hypertension Clinical types of GN Glomerulonephropathy Confined conceptleading manifestation: proteinuria, with/without hematu

18、riaExtensive conceptglomerular diseases ( disorders ) Glomerulonephritisleading manifestation: hematuria, with/without proteinuriaNephrotic syndrome 1. Large-amount proteinuria 2. hypoalbuminemia 30g/L 3. edema 4. hyperlipidemia 1+2 -essentialsevere edemahyperlipidemiahypoalbuminemiaLarge-amount pro

19、teinuriaCenter keyEssential for diagnosisIntake of protein Ingestion from GIsynthesis in liverlost through urineNSconsumptionMechanisms of hypoalbuminemiaLinkage of clinical manifestation and pathological changes (1)Pathological proliferative non-proliferativechanges MsPGN MCD MmPGN MN* Endocapillar

20、y PGN FSGS Crescentic GNClinical hematuria proteinuria certain certain, sometimesManifestation nephritis syndrome nephrotic syndrome proteinuria hematuria possible occasional * Linkage of clinical manifestation and pathological changes (2) clinical pathological AGN endocapillary PGN possible NS RPGN

21、 crescentic GN possible NS CGN nephritis syndrome MsPGN 2 MmPGN 2 nephritis syndrome FSGS 2 +nephrotic syndrome MN2 NS MCD 1 Acute GlomerulonephritisEtiologyStreptococcus -hemolytic streptococcus, group A, type XII, nephritogenic strainsantigencomponents of cytoplasm & membranefrequently CIC, someti

22、mes planted antigenOthersother bacteria, such as staphylococcus epidermidisvirusesparasitesPathological changes Endocapillary Proliferative GN Acute phase Proliferation of endothelial & mesangium Recovery phase Only mesangium proliferation, sometimes minor lesion Clinical Manifestation1.Epidemiology

23、: primarily children, sometimes adults & the aged2. Preliminary infectionfrequently tonsillitis,upper respiratory infectionLatent period:1-3 woccasionally skin infectionLatent period:longer,but less than 4w3.Nephritis syndrome(1)hematuria 100%，40% are gross hematuria(2)proteinuria frequent，90%(4)hyp

24、ertension 80%(5)renal failure mild,acute renal failure4.Laboratory findings acute phase of infection of Strep.elevated ASO titer (some Strep. No hemolysin O)only the marker of infection, not nephritis(2) acute phase of immune reactionsserum C3 & total complements,return to normal within 8wblood CIC

25、Natural Historyedema and hypertension disappear in one monthhematuria, proteinuriausually reduce in one month, resolve within 2 to 3 monthssome resolve within 6 to 12 monthsC3return to normal in two monthsDiagnosisPointspreliminary infection &latent periodacute onsetsurely hematuria, frequently edem

26、a and hypertensionASO , C3 dynamic changeSelf-limitation Differential DiagnosisDiseases presented with acute nephritis syndrome GN secondary to infection of other pathogensother bacteria, viruses (Varicella-zoster virus, EB, influenza virus)Climax of infection or within 5 daysMild abnormal of urine

27、examinationHypertension and edema are unusual Normal blood complement level rapidly progressive GN CGN systemic diseases lupus nephritis Schnlein-Henoch purpuraIndications of kidney biopsyOligouria 1w，except ECBV insufficient, urinary tract obstruction, etcProgressive renal failureUnresolved in 2 mo

28、nthsuntypical manifestation, or with nephrotic syndromeTreatment1.Supportive treatment Rest Food & waterRestrictive intake ofNaCl 5 g/dif moderate to severe edema or hypertensionWaterif decreased urine volume ProteinRenal failure, but not dialysis yet2.Treatment of infectionPenicilin for 2 wTonsille

29、ctomy if recurrent attacks of tonsillitispatients condition is stable, Upro1g/d, URBC 10/HPPenicilin for 2 wks before and after the surgery3. Symptomatic treatmentDiuresisAntihypertensionDialysisPrognosis hematuria, proteinuriausually reduce in one month, resolve within 2 to 3 monthssome resolve wit

30、hin 6 to 12 months 1%ARF Death 6%-18% CGN?Rapidly progressive glomerulonephritisRPGN Rapidly progressive nephritis syndromeSome induced by respiratory infectionAcute onset, rapidly progressiveRenal failure within a few weeks to a few months 1.primary RPGN Crescentic GN2.other primary GN other pathol

31、ogical changes with lots of crescents3.secondary RPGN SLE, SHP, etc RPGN Type I Type II Type III anti-GBM IC Pauci-immuneIF linear GBM Granular GBM - deposits & mesangium deposits anti-GBM AB+C3、CIC 70%-80% small vessel vasculitis ANCA + the young & the middle-aged the middle-aged middle aged & aged

32、 & aged Most frequently in ChinaDiagnosisAcute onsetRapidly progressiveRenal failure within a few weeks to a few monthsAcute renal failure Chronic renal failureDifferential Diagnosis Rapidly progressive nephritis syndrome not primary RPGN - other primary GN AGN, IgAN, etc - secondary GN Goodpasture

33、Syndrome, LN, SHP * accompanied by crescentic GN * severe pathological changes Diseases with ARFATNAIN - definite etiology -obsolete proteinuria and hematuria - specific manifestation ATNlarge quantity of renal tubular epithelial cells in urine AINhypersensitiveness (rashes, fever, arthralgia) Treat

34、ment EARLY! Aim to humoral immune mechanisms 1.plasmapheresis discard the antibodies plasm exchange immoadsorption type I, III 2.drugs glucocorticoid +cytotoxic drugs3，repeat if necessary CTX type II, IIIsymptomatic treatment renal failurebalance of fluid, electrolytes and acid-basedialysis infectio

35、n hypertensionPrognosis Hardly relieve mostCRF or deathRisk factors Type I-worst,II-worse,III-bad Treatment not progressive & prompt Age the aged Chronic GlomerulonephritisManifestation chronic nephritis syndromePathological changes except MCD,MmPGN, Crescentic GNClinical manifestation any age, freq

36、uently young 2.preliminary infection upper respiratory tract, intestinal tract latent period 1 wk 3.nephritis syndrome Hematuria,proteinuria,edemaHypertension,renal failureuremia4.Prognosis factors (1)pathological properties (2)treatment (3)hypertension (4)infection,prerenal factors (hypotension etc

37、) (5)nephrotoxic drugsPoints of Diagnosis chronic onset proteinuria and/or hematuria protracted and progressive Differential DiagnosisCGNDifferential Diagnosis 1. AGN AGN CGN age children young&middle-aged preliminary infection frequently sometimes latent period 1-3w dialation of afferent glomerular

38、 arteriole pressure in glomeruli Upro postpone glomerulosclerosis ACEI/ARB 3.anti-platelet 4.immunosupression Clinical manifestation (1)large quantity of Upro (2)severe edema (3)hypoalbuminemia (4)hyperlipidemia Nephrotic Syndrome2.Others (1) thrombosis & embolism renal veins or inferior vena cava 2

39、5% (2)infection (3)acute renal failureBlood volumeperfusion of kidneys ischemia of kidneys, tubule necrosisSevere glomerular lesionscrescent formationSevere proliferation of mesangiumNecrosis of capillary loopsNephrotoxic drugsidiopathetic 1.among varied types of pathology 2.between secondary GN1SLE

40、2SHP3DN history, hematuria, pathological changes4amyloidosis history of chronic infection,systemic lesions (heart, liver, GI, tongue), pathological changes (kidney, tongue, rectum)5MM Middle-aged/aged, ostalgia, osteonecrosis(X-ray, isotope scanning), abnormal protein (blood single-peak protein, blo

41、od and urine light chain protein,urine BJ protein)Diagnosis & Differential Diagnosis 1. Supportive treatment 1. rest 2. Food and water (1) water & sodium restriction when with severe edema (2) protein (3) lipid restriction when with hypoalbuminemia (4) energy 30-35 Kal/kg/dTREATMENT2. symptomatic tr

42、eatment 1. diuresis osmotic diuretics plasma colloid osmotic pressure tubule fluid osmotic pressure fluid transmit from tissue readsorption of water space to blood vessels blood volume diuretics mannitol, dextran, albumindiuresis2. Aim to proteinuria ACEI/ARB3. Major treatment 1. glucocorticoid mech

43、anisms (1)immuosupression (2)anti-inflammation principles (1)sufficient dose when initiation reduce 2wks after Upro is negative *if Upro doesnt reduced apparently in 8-12wksineffective (2) reduce the dose slowly 10%/2-3wks (3) sustaining treatment minimal dose:10-15mg/d，6m-1y Sensitivity of glucocor

44、ticoid 1mg/kg/d 8w negative Upro positive relapse when reduce to some dosage sensitivedependentineffective2. immunosuppressive agents cytotoxic drugs alkylating agentCTX, chlormethine, CB1348 inhibit duplication of DNA Aza,MMF inhibit synthesis of RNA inhibit proliferation of B lymphocyte CyA inhibi

45、t synthesis of L-2 inhibit proliferation of T lymphocyteindications glucocorticoid dependent or ineffective glucocorticoid untolerated4. Treatment of complications anticoagulation, thrombolysis anti-infection balance of electrolyte 我劝一个草率结婚的朋友离婚。她平静的告诉我，如果说当初鲁莽结婚是个错误。那么，现在草率离婚是一错再错。这位朋友后来还是离婚了，大家一致认

46、为她的行为很理性。同样的故事正在互联网搜索巨头谷歌身上发生，但是谷歌选择了草率“离婚。饮鸩止渴由于急于抑制苹果iphone 翻天覆地的产业冲击，谷歌采取急功近利的粗糙型开放策略。饮鸩止渴的策略一时取得了成果。市场研究公司尼尔森最近公布的数据显示，在通过Verizon Wireless、AT&T和Sprint Nextel三大运营商经销后，谷歌Android 在美国市场上的销售量已经超过iPhone。另一家市场研究公司iSuppli甚至认为，全球范围内使用Android操作系统的 数量将在 2021年超过苹果iPhone。 外表繁华的背后，是Android生态系统的一团糟，谷歌正在为自己的粗放型

47、开放策略买单。用户对谷歌 的态度从开始的好奇、后来的犹豫，变成强烈的批评。“大多Android 程序都是垃圾，乱七八糟的，一位 发烧友迅速投奔了iphone的阵营：“同样的植物人大战僵尸游戏，在谷歌 和iphone 上的体验简直没法比混乱，还是混乱。一切一切的乱象，折射出谷歌已经失去对Android生态系统的控制。这一切的根源，我的判断是开放策略初期过于宽松，导致失去控制权。混乱的生态系统表现在用户 上，就是应用程序的混乱和粗燥。一错再错为此，谷歌开始采取对策。最近，有国内厂商称新的开始关闭应用程序的API(应用程序编程接口)，统一Android界面。这意味着，谷歌将放弃其初始开放策略，开始封

48、闭管理。粗看之下，谷歌认识到自己的错误。既然是过度开放导致的错误，那么收紧开放尺度是很自然的逻辑，无懈可击。但我认为，谷歌仓促收紧开放策略仍然是个错误。打个比喻。如果过度开放的政策是草率结婚，那么草率的封闭就是草率离婚。这么判断的原因很简单，谷歌把Android开放出去的那一天，Android已经不属于谷歌。谷歌没有认识到这一点，还以为Android只是自己的。合作伙伴对谷歌封闭政策的反响加强了我的判断结论。经济观察报报道，国内第一家生产基于Android平台 的设计公司创杨通信，近日已经被迫出售。创杨通信负责人给出的出售理由是，“因为不愿意甘当炮灰而选择放弃。按照目前将统一界面的想法，未来的

49、 市场将出现毫无差异化的产品。这对于企业来说，几乎意味着不可防止的价格战。利润空间的微薄，导致合作伙伴生存环境恶劣。于是大量退出几乎是一种必然。除了为合作伙伴找到新的利益空间，谷歌还将面临开放阵营精神层面的声讨，这对谷歌的挑战会更大。如果说谷歌为了自己竞争的私利利用了开放，赢得了名声。那么，谷歌不能一脚把开放踢开，他现在还需要为这种名声买单。如果只顾自己收网，谷歌会被面临铺天盖地的道德谴责。谷歌，希望你准备好了，三思而行。木桶效应就是指一个水桶无论有多高，它盛水的高度取决于其中最低的那块木板。这在选购 的时候也同样适用。尤其是很多用户在购置 的时候， 都会专注于某一个参数，比方要求处理器主频要

50、高达1GHz，但一部 的整机表现是由多个因素组成，所以在购置 的时候一定要从整体的角度上来看一部手 机的性除了处理器主频以外，其实还有很多影响整机表现的元素，比方运行内存(RAM)、机身内存(ROM)、操作系统、厂商对系统的优化都会有所影 响。不过在很多用户眼中，这几项却远没有处理器主频重要。而如果忽略这几项的话，可能买到一个主频很高，但整机性能却仍然不令人满意的机型。用户在-财务部员工 老子不求人，人人求老子！于是乎，这帮狗屎们天天拽得好似自己是救世主是其他员工的再生父母一样，牛！超级牛！100牛！我活这么大了还真没看到过不牛的财务，这帮人其实在公司是同事们最不敢得罪、但更是最让人看不起，人

51、际关系最差的一群人，当然，据我观察，也是离婚率最高的一类人。 最有城府最有心计的人-人力资源部员工 每天的工作就是算计如何搞出用最小代价换取最大回报的提议来讨好老板，看谁不顺眼就想方设法算计如何在考核、薪酬奖金分配方面给他穿小鞋的鸟人。：智商最高情商最差的人-研发部员工 技术过硬，为人木衲。上台发言三分钟 搞不出一句话来，向领导汇报工作结结巴巴没 更多精品文档请访问我的个人主页 :/ docin /611696569谢，再见！个半小时理不出个头绪来。企业中最好管理的一群伪知识分子，可以被任意剥削，根本上不会对抗，或者从来就没有过对抗的意识 最吊儿郎当和无耻的人-销售部员工 老板们财富的来源，老

52、板们最想讨好的一群人，这群人其实也是最无耻公司内口碑最差却又人际关系最和谐的一群人。天天吊儿郎当的来公司报个到，调戏一下前台，和狐朋狗友打打 ，10点不到就开始琢磨找借口出门拜见客户，其实下午就是上 所述，大家在选购 的时候一定要综合考虑一款 的硬件规格。除此之外，也不要把硬件看的太过重要，就比方苹果iPhone 3GS在硬件配置上并不出众，但却在操控手感以及软件资源上目前难有机型企及。更高分辨率能获得更为逼真细腻的显示效果，所以对于屏幕的分辨率绝大多数人都会偏向于分辨率更高的机型。但对于笔者 所说的高分辨率未必是好事会有所疑心。其实这里说的高分辨率“不好更多是指采用非主流的高分辨率机型。在此

53、前，就有几款“悲情机型在分辨率上吃了不小 的亏。大名鼎鼎的HTC Diamond就是一款颇具代表意义的机型，Diamond上市的 市场还处于QVGA时代、只有少数旗舰机皇采用WVGA这样级别的屏幕，由于HTC Diamond却采用了VGA这一过渡型的分辨率，而也正是因为这一点，Diamond很多软件都未有支持或无法完美运行，可谓是一个不小的遗憾。除此之 外，曾经非常经典的 附赠人生心语人生太短，聪明太晚人生太短，聪明太晚(1)我们都老得太快却聪明得太迟把钱省下来，等待退休后再去享受结果退休后，因为年纪大，身体差，行动不方便，哪里也去不成。钱存下来等养老，结果孩子长大了，要出国留学，要创业做生意

54、，要花钱娶老婆，自己的退休金都被拗走了。人生太短，聪明太晚(2)当自己有足够的能力善待自己时，就立刻去做，老年人有时候是无法做中年人或是青少年人可以做的事，年纪和健康就是一大因素。小孩子从小就告诉他，养你到高中，大学以后就要自立更生，要留学，创业，娶老婆，自己想方法，自己要留多一点钱，不要为了小孩子而活我们都老得太快却聪明得太迟，我的学长去年丧妻。这突如其来的事故，实在叫人难以接受，但是死亡的到来不总是如此。学长说他太太最希望他能送鲜花给他，但是他觉得太浪费，总推说等到下次再买，结果却是在她死后，用鲜花布置她的灵堂。这不是太蠢愚了吗？！等到.、等到.，似乎我们所有的生命，都用在等待。人生太短，

55、聪明太晚(3)等到我大学毕业以后，我就会如何如何我们对自己说等到我买房子以后！等我最小的孩子结婚之后！等我把这笔生意谈成之后！等到我死了以后人人都很愿意牺牲当下，去换取未知的等待；牺牲今生今世的辛苦钱，去购置后世的安逸在台湾只要往有山的道路上走一走，就随处都可看到农舍变精舍，山坡地变灵塔，无非也是为了等到死后，能图个保障，不必再受苦。许多人认为必须等到某时或某事完成之后再采取行动。明天我就开始运动，明天我就会对他好一点，下星期我们就找时间出去走走；退休后，我们就要好好享受一下。人生太短，聪明太晚(4)然而，生活总是一直变动，环境总是不可预知，现实生活中，各种突发状况总是层出不穷。身为一个医生，

56、我所见过的死人，比一般人要来得多。这些人早上醒来时，原本预期过的是另一个平凡无奇的日子，没想到一个意料之外的事；交通意外、脑溢血、心脏病发作等等。剎那间生命的巨轮倾覆离轨，突然闯进一片黑暗之中。那么我们要如何面对生命呢？我们毋需等到生活完美无瑕，也毋需等到一切都平稳，想做什么，现在就可以开始做起。一个人永远也无法预料未来，所以不要延缓想过的生活，不要吝于表达心中的话，因为生命只在一瞬间。人生太短，聪明太晚(5)记住！给活人送一朵鲜花，强过给死人送贵重的花圈，每个人的生命都有尽头，许多人经常在生命即将结束时，才发现自己还有很多事没有做，有许多话来不及说，这实在是人生最大的遗憾。别让自己徒留为时已

57、晚的空余恨。逝者不可追，来者犹未卜，最珍贵、最需要实时掌握的当下，往往在这两者蹉跎间，转眼错失。人生太短，聪明太晚(6)人生短暂飘忽，包得有一首小诗这样写：高天与原地，悠悠人生路；行行向何方，转眼即长暮。正是道尽了人生如寄，转眼即逝的惶恐。有许多事，在你还不懂得珍惜之前已成旧事；有许多人，在你还来不及用心之前已成旧人。遗憾的事一再发生，但过后再追悔早知道如何如何是没有用的，那时候已经过去，你追念的人也已走过了你。人生太短，聪明太晚(7)一句瑞典格言说：我们老得太快，却聪明得太迟。 不管你是否觉察，生命都一直在前进。人生并未售来回票，失去的便永远不再得到。将希望寄予等到方便的时间才享受人生太短，

58、聪明太晚(8)我们不知失去了多少可能的幸福不要再等待有一天你可以松口气，或是麻烦都过去了。生命中大局部的美好事物都是短暂易逝的，享受它们、品尝它们，善待你周围的每一个人，别把时间浪费在等待所有难题的完满结局上。找回迷失的生命死亡也许是免费的 但是，却要付出生命的代价。劝大家一句话：把握当下，莫等待。成功人生的十堂课人生成功第1课 做一个终生学习的人，离开学校并不意味着学习就结束了。学习可以成为一种生活方式，帮助你发挥最大的潜能。我们从未停止学习，总会有新的，有趣的东西等待我们去发现。学习新的技能可能让人感到有一点恐惧，但每当我们在个人学习上停滞不前时，我们都需要去学习新的东西。积极地寻求支援和

59、建议，突破停滞期。【大学课件】出品版权归原作者所有!参加一些培训，进修，夜校任何新的兴趣都将会有助于开展你的优势。多看，多听，让你的头脑保持活泼。活到老，学到老。 人生成功第2课 令自己感到沮丧的秘诀就是用空闲时间去烦恼自己是否快乐。所以不要费事去想它！摩拳擦掌干起来吧。你将热血沸腾，你会头脑清醒。很快，在你身体中的这种高涨的积极人生观将把烦恼从你的头脑中赶出去。行动起来，忙碌起来。这是世界上最廉价的一种药，也是最好的一种。人生成功第3课 在困境中寻找成功的希望逆境是一所最好的学校。每一次失败，每一次打击，每一次损失，都蕴育着成功的萌芽，都教会我在下一次有更出色的表现。我再也不会逃避现实，也不

60、会拒绝从以往的错误中获取经验，我不再因此而促成自己的失败。因为我知道，宝玉不经磨砺就不能发光，没有，我也不能完善自我。现在我知道，灵魂倍受煎熬的时刻，也正是生命中最多项选择择与时机的时刻。任何事情的成败取决于我在寻求帮助时是抬起头还是低下头。无论何时，当我被可怕的失败击倒，在最初的阵痛过去之后，我都要想方设法将苦难变成好事。伟大的机遇就在这一刻闪现这苦涩的根必将迎来满园芬芳！ 我将一直在困境中寻找成功的希望。 人生成功第4课 没有人可以使你感到自卑我选择自我感觉良好，这样我能更加开放地学习。如果人们给我负面的回应或是批评我做的事情，我不会认为他们所说的就说明我是一个“差劲的人。我坚信自尊由我掌