1、精品PPT课件 浏览免费 下载后可以编辑修改。 http:/ http:/ http:/ http:/ http:/ syndrome,Figure 1. Nephrotic edema.,Figure 2. Nephrotic edema.,Clinical Syndrome,肾脏及泌尿系疾病经常会引起一些临床症状、 体征和实验室表现相似的综合征。识别患者属于哪一种综合征对诊断很有帮助，因为导致每个综合征的病因较之其包含的个别临床症状和体征的致病原因要少，故识别患者属于哪一种综合征对诊断有帮助。,The most common syndrome of kidney disease,Nephr
2、otic syndrome Nephritic syndrome Asymptomatic urinary abnormalities Acute renal failure or Rapidly progressive renal failure Chronic kidney disease(Table 1),(一)肾病综合征 (二)肾炎综合征 (三)无症状性尿检异常 (四)急性及急进性肾衰竭综合征 (五)慢性肾脏病(表1),肾脏疾病常见综合征,Table 1. STAGES OF CHRONIC KIDNEY DISEASE*,* Chronic kidney disease is def
3、ined as either kidney damage or GFR 60mL/min/1.73m2 for 3months. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or image studies.,Nephrotic syndrome,This is characterized by proteinuria (Typically 3.5g/24h),hypoalbuminemia (
4、 less than 30g/dL ) and edema. Hyperlipidaemia is also present.Primary and secondary causes are summarized in Table 2, 3In practice, many clinicians refer to “nephrotic range” proteinuria regardless of whether their patients have the other manifestations of the full syndrome because the latter are c
5、onsequences of the proteinuria.,NEPHROTIC SYNDROME,Pathophysiology Proteinuria Hypoalbuminemia Edema HyperlipidemiaCause (diagnosis and differential diagnosis) Systemic renal disease hepatitis B associated glomerulonephritis, Henoch-Schonlein purpura, systemic lupus erythematosus, diatetes mellitus,
6、 amyloidosis Idiopathic nephrotic syndromeComplications Infection Coagulation disorders Protein malnutrition and dyslipidemia Acute renal failure,Pathophysiology,Proteinuria,Proteinuria can be caused by systemic overproduction, tubular dysfunction, or glomerular dysfunction. It is important to ident
7、ify patients in whom the proteinuria is a manifestation of substantial glomerular disease as opposed to those patients who have benign transient or postural (orthostatic) proteinuria.,Heavy proteinuria (albuminuria),Figure 3.,Hypoalbuminemia,Hypoalbuminemia is in part a consequences of urinary prote
8、in loss. It is also due to the catabolism of filtered albumin by the proximal tubule as well as to redistribution of albumin within the body. This in part accounts for the inexact relationship between urinary protein loss, the level of the serum albumin, and other secondary consequences of heavy alb
9、uminuria .,The salt and volume retention in the NS may occur through at least two different major mechanisms. In the classic theory, proteinuria leads to hypoalbuminemia, a low plasma oncotic pressure, and intravascular volume depletion. Subequent underperfusion of the kidney stimulates the priming
10、of sodium-retentive hormonal systems such as the RAS axis, causing increased renal sodium and volume retention, In the peripheral capillaries with normal hydrostatic pressures and decreased oncotic pressure, the Starling forces lead to transcapillary fluid leakage and edema .,Edema,In some patients,
11、 however, the intravascular volume has been measured and found to be increased along with suppression of the RAS axis. An animal model of unilateral proteinuria shows evidence of primary renal sodium retention at a distal nephron site, perhaps due to altered responsiveness to hormones such as atrial
12、 natriuretic factor. Here only the proteinuric kidney retains sodium and volume and at a time when the animal is not yet hypoalbuminemic. Thus, local factors within the kidney may account for the volume retention of the nephrotic patient as well.,Edema,Figure 4.,Hyperlipidemia,Most nephrotic patient
13、s have elevated levels of total and low-density lipoprotein (LDL) cholesterol with low or normal high-density lipoprotein (HDL) cholesterol . Lipoprotein (a) Lp(a) levels are elevated as well and return to normal with remission of the nephrotic syndrome. Nephrotic patients often have a hypercoagulab
14、le state and are predisposed to deep vein thrombophlebitis, pulmonary emboli, and renal vein thrombosis.,Cause,Table 2 CAUSES OF THE NEPHROTIC SYNDROME,Table 3a NEPHROTIC SYNDROME ASSOCIATED WITH SPECIFIC CAUSES (“SECONDARY” NEPHROTIC SYNDROME),Table 3b NEPHROTIC SYNDROME ASSOCIATED WITH SPECIFIC CA
15、USES (“SECONDARY” NEPHROTIC SYNDROME),Pathology patterns and clinical presentations of idiopathic nephrotic syndome,In adults, the nephrotic syndrome is a common condition leading to renal biopsy. In many studies, patients with heavy proteinuria and the nephrotic syndromes have been a group highly l
16、ikely to benefit from renal biopsy in terms of a change in specific diagnosis, prognosis, and therapy. Selected adult nephrotic patients such as the elderly have a slightly different spectrum of disease, but again the renal biopsy is the best guide to treatment and prognosis (Table 2, 3).,Renal biop
17、sy,PRIMARY NEPHROTIC SYNDROME,Minimal Change DiseaseFocal Segmental GlomerulosclerosisMembranous NephropathyMembranoproliferative Glomerulonephritis (MPGN),Figure 5a. Pathology of glomerular disease. Light microscopy. (a) Normal glomerulus; minimal change disease.,Table 4,PRIMARY NEPHROTIC SYNDROME,
18、Minimal Change DiseaseFocal Segmental GlomerulosclerosisMembranous NephropathyMembranoproliferative Glomerulonephritis(MPGN),Figure 5b. Segmental sclerosis; focal segmental glomerulosclerosis.,Figure 6. Light microscopic appearances in focal segmental glomerulosclerosis. Segmental scars with capsula
19、r adhesions in otherwise normal glomeruli.,Table 5,PRIMARY NEPHROTIC SYNDROME,Minimal Change DiseaseFocal Segmental GlomerulosclerosisMembranous NephropathyMembranoproliferative Glomerulonephritis(MPGN),Figure 7a. Early MN: a glomerulus from a patient with severe nephrotic syndrome and early MN, exh
20、ibiting normal architecture and peripheral capillary basement membranes of normal thickness (Silvermethenamine 400).,Figure 7b morphologically advanced MN,Figure 7c. Morphologically more advanced MN (same patient as in (b),Table 6,PRIMARY NEPHROTIC SYNDROME,Minimal Change DiseaseFocal Segmental Glom
21、erulosclerosisMembranous NephropathyMembranoproliferative Glomerulonephritis(MPGN),Figure 8. Pathology of membranoproliferative glomerulonephritis type I. (a) Light microscopy shows a hypercellular glomerulus with accentuated lobular architecture and a small cellular crescent (methenamine silver).,T
22、able 7,Diagnosis and Differential diagnosis,Initial evaluation of the nephrotic patient includes laboratory tests to define whether the patient has primary, idiopathic nephrotic syndrome or a secondary cause related to a systemic disease.,Common screening tests include the fasting blood sugar and gl
23、ycosylated hemoglobin tests for diabetes, and antinuclear antibody test for rheumatoid disease, and the serum complement, which screen for many immune complex-mediated disease (Table 3), In selected patients, cryoglobulins, hepatitis B and C serology, anti-neutrophil cytoplasmic antibodies (ANCAS),
24、anti GBM antibodies, and other tests may be useful. Once secondary causes have been excluded, treating the adult nephrotic patient often requires a renal biopsy to define the pattern of glomerular involvement.,It leads to a multitude of other consequences , such as predisposition to infection and hy
25、percoagulability. In general, the diseases associated with NS cause chronic kidney dysfunction, but rarely they can cause ARF. ARE may be seen with minimal change disease, and bilateral renal vein thrombosis.,Complications,Infection Coagulation disorders Protein malnutrition and dyslipidemia Acute r
26、enal failure,Treatment 治疗,1. General treatment 2. Symptomatic treatment (e.g.diuresis to relieve edema, treating dyslipidemias, anticoagulate treatment, etc.) 3. Immunosupressive treatment,一、一般治疗 二、利尿消肿 三、免疫抑制治疗 四、调脂药物 五、抗凝治疗,Thank you,严重患者发生急性糜烂性胃炎的病理机制可能为胃粘膜屏障功能减弱。胃粘膜的血流减少和可能伴有的酸分泌增加(如烧伤，中枢神经系统创伤和
27、败血症)可促进粘膜炎症和溃疡的形成。 症状、体征和诊断：通常，患者可能因为病情太重而说不清胃部症状，即使症状存在，常是轻度的和非特异性的。首发的明显体征常为在鼻胃吸引时出现血液，一般发生在严重应激反应的最初25天内。 内镜检查可明确诊断，某些患者(如烧伤，休克和败血症)在急性损伤12小时内可发生急性糜烂。病灶多从胃底部开始，呈瘀点或瘀斑，逐渐融合成220mm不规则的小溃疡，出血极为少见，组织学病变局限于粘膜，经处理或除去应激后可迅速愈合。病灶可继续发展，累及粘膜下层，甚至穿透浆膜，更为常见的是胃底部发生多处出血，胃窦部也可被累及。头部损伤与其他情况不同，此时胃酸分泌不是减少，而是增加，病灶(C
28、ushing溃疡)可为孤立，也可累及十二指肠。 预防和治疗：据报道，患者一旦发生严重出血(约见重症监护病房患者的2%)，死亡率可达60%以上。大量输血会进一步削弱止血。虽然各种手术和非手术方法如抗分泌的溃疡药物，血管收缩剂，血管造影技术(如动脉栓塞)，内镜下凝固疗法已被采用，但效果并不理想。除全胃切除外，其他手术后的继续出血是常见的，且死亡率与内科治疗相同。 主体部分要一一列出准备开展的工作(学习)、任务，并提出步骤、方法、措施、要求。这 是计划最重要的内容，也是篇幅最大的一部分。通常主体部分由于内容繁多，需要分层、分 条撰写。常见的结构形式为：用“一、二、三”的序码分层次，用“(一)、(二)、 (三)”加“123”的序码分条款。具体如何分层递进，依内容的多少及其 内在的逻辑性而定，可参考后附例文。 3结尾 结尾可以用来提出希望、发出号召、展望前景、明确执行要求等，也可以在条款之后就结束 全文，不写专门的结尾部分。 所以让人看明白为什么要这么去做这件事情，就是策划要做的事情。,精品课件文档,本文档下载后可以修改编辑，欢迎下载收藏。,
