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当治疗不彻底、不规则时，耐药菌株存在或机体免疫力减低时出现，临床无发热等毒血症表现，粪便性质也不典型，可为消化不良稀便，甚至软便或有黏液，间有少量脓冻、脓血便，次数多少不定。 | [
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"entity": "消化不良稀便",
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"entity": "软便",
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"entity": "有黏液",
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"entity": "脓血便",
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【并发症】脱水是最常见的，它可引起肾衰竭和死亡。 | [
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当发生休克、毒血症时死亡率可高达20%～50%。 | [
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此外，在志贺菌感染时，溶血性尿毒症综合征是较常见的并发症。 | [
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另外，脱肛、中毒性巨结肠、肠穿孔、伪膜性结肠炎、严重营养不良所致结膜炎、虹膜炎、角膜溃疡等为不常见的并发症。 | [
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"entity": "肠穿孔",
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"entity": "伪膜性结肠炎",
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"entity": "严重营养不良",
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"entity": "结膜炎",
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"entity": "虹膜炎",
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"entity": "角膜溃疡",
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【诊断】有典型的脓血便，结合临床表现和流行季节，诊断并不困难。 | [
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实验室检查粪便镜检有大量白细胞、脓细胞或红、白细胞。 | [
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"entity": "大量白细胞、脓细胞或红、白细胞",
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血常规白细胞增加明显，并有核左移，都支持诊断。 | [
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大便和直肠拭子细菌培养是最好的诊断方法。 | [
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最近已开展PCR快速诊断法。 | [
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【鉴别诊断】具有脓血便，在儿科应与鼠伤寒杆菌肠炎、金黄色葡萄球菌肠炎、真菌性肠炎和出血坏死性小肠炎鉴别。 | [
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"entity": "金黄色葡萄球菌肠炎",
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"entity": "真菌性肠炎",
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"entity": "出血坏死性小肠炎",
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无典型脓血便者，特别是婴幼儿菌痢需与致病性大肠埃希菌肠炎、病毒性肠炎、空肠弯曲菌肠炎鉴别。 | [
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中毒性菌痢应与暴发型流脑、乙型脑炎、大叶性肺炎及其他病原菌引起的感染性休克鉴别。 | [
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慢性菌痢应与慢性非特异性溃疡性结肠炎、慢性血吸虫病相鉴别。 | [
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2.控制感染抗生素治疗目前对抗生素耐药的痢疾杆菌株的地理分布是不同的。 | [
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对敏感株，氨苄西林口服100mg/（kg•d），每天分四次口服即可。 | [
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阿莫西林效果不如氨苄西林，但胃肠道吸收好。 | [
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由于复方磺胺甲唑在我国耐药率较高，它不用做首选用药头孢克肟（cefixime）8mg/（kg•d），口服分两次，共服5天，或口服其他三代头孢菌头孢曲松（cetriaxone）50mg/（kg•d），每天一次，肌内注射或静脉注射2～5天，可作为首选。 | [
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"entity": "静脉注射",
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萘啶酸（nalidixic）55mg/（kg•d）分四次给予，共用5天，是另一种替代方法，疗程一般5天。 | [
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口服一、二代头孢菌素不能作为二线替代药。 | [
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吡哌酸因对小儿骨骼发育有影响，18岁以下慎用。 | [
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3.中毒性菌痢治疗根据临床不同表现对症治疗。 | [
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4.慢性菌痢采用支持疗法和抗病原治疗相结合，应2种以上抗生素联合用药和药物保留灌肠。 | [
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【预防】1.痢疾高发地区应鼓励延长母乳喂养。 | [
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2.指导幼儿园、学校的儿童及工作人员及时进行清洁和消毒工作。 | [
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3.作好疫情报告，出现疫情后，立即找出并控制传染源，禁止患者或带菌者从事餐饮业和保育工作。 | [
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第五节肢体保留性治疗长期以来，恶性骨肿瘤的治疗中，截肢一直被推崇为外科治疗的主要手段。 | [
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近10多年来，一种既考虑到恶性骨肿瘤的有效治疗，同时又尽量兼顾保留患肢的治疗方法正在兴起并得到了很多学者的重视和采用。 | [
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这就是肢体保留性治疗肢体保留性治疗（limbsalvage），简称保肢治疗。 | [
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保留有功能而无肿瘤的肢体是保肢治疗的根本。 | [
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因此，治疗前仔细的计划和肿瘤分期，明确局部病灶的切除范围，包括手术前后的化疗都对治疗的结果有着很重要的影响。 | [
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保肢治疗不是适用于所有骨肿瘤病人的通用治疗方法，必须因人而异，根据不同的病人采用各自适用的保肢方法，具体对待不同的分期和类型的肿瘤。 | [
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施行保肢治疗，在现阶段条件下的确也还存在着许多潜在的危险和并发症，有时要达到一个稳定有功能的肢体，可能需要两次甚至多次的手术。 | [
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因此，截肢手术远没有走到应该放弃的地步。 | [
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施行肢体保留性治疗的条件：①肿瘤处于发病的早期；②肿瘤边缘清楚，可以施行外科切除，并有把握保护好手术中对坐骨神经和其分支等重要结构的损伤；③手术前必须充分考虑好手术后切除部位的皮肤覆盖问题，避免术后无组织局部的皮肤坏死；④有经验的骨科医生。 | [
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}
] |
保肢治疗的主要方法为：1.肿瘤局部切除手术中广泛切除肿瘤组织和覆盖肿瘤的软组织。 | [
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"entity": "保肢治疗",
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"entity": "软组织",
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采用髓内或髓外固定，并辅以自体植骨的方法，固定长骨中段的缺损，使切除两端的骨组织重新连接。 | [
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{
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"entity": "骨组织",
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2.同种异体骨关节重建肿瘤切除后采用同种异体关节移植重建骨关节功能，但是供体来源的有限、植入体连接困难和骨折以及关节软骨的退化和塌陷大大限制了这种方法的广泛使用。 | [
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"id": 0,
"entity": "同种异体骨关节重建",
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{
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{
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{
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{
"id": 5,
"entity": "软骨的退化和塌陷",
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3.人工关节假体功能重建这是肢体保留治疗中采用最多的一种方法。 | [
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随着人工关节假体材料技术和植入技术的日渐成熟，这种新的治疗方法正在越来越多的显示出其在恶性骨关节肿瘤中的应用优势。 | [
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根据患者实际尺寸定制或采用通用型的人工关节，安装在肿瘤切除后的关节进行重建。 | [
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{
"id": 1,
"entity": "关节",
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对于儿童病例，考虑到肢体的继续生长趋势，目前已有可生长性的假体问世，为这种新的治疗方法带来了希望。 | [
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第二节慢性肾衰竭慢性肾衰竭（chronicrenalfailure，CRF）是指各种原因造成的慢性进行性肾实质损害，呈进行性不可逆转的肾小球滤过率下降，导致氮质血症、代谢紊乱和各系统受累的临床综合征。 | [
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{
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"entity": "代谢紊乱",
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"label": "dis"
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当进展到需肾透析或移植方可维持生命时称为终末期肾病（endstagerenaldisease，ESRD）。 | [
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CRF小儿中的发生率国内尚无确切数据，国外报道为每百万人口中4～5人。 | [
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【病因】慢性肾衰竭的病因以各种原发性及继发性肾小球肾炎占首位，其次为泌尿系统先天畸形（如肾发育不良，先天性多囊肾，膀胱输尿管反流等）及遗传性疾病（如遗传性肾炎，肾髓质囊性病，Fanconi综合征等）。 | [
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"entity": "遗传性肾炎",
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{
"id": 9,
"entity": "Fanconi综合征",
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] |
全身性系统疾病中以肾小动脉硬化、高血压及结缔组织病等多见。 | [
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{
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] |
近年来肾间质小管损害引起的CRF也逐渐受到人们的重视，糖尿病肾病、自身免疫性与结缔组织疾病及肾损害引起的CRF也有上升趋势。 | [
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{
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{
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"entity": "CRF",
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Topel统计欧洲37个肾移植中心总结286例＜15岁儿童肾移植病例其终末期肾病的分布：慢性肾小球肾炎52.3%，慢性肾盂肾炎20.8%，遗传性肾病8.0%，血管性肾病4.5%，多囊肾3.0%，药物性肾病2.4%，先天性肾发育不全1.6%，其他（包括胱氨酸沉积症、草酸盐沉积症、Alport综合征及溶血尿毒综合征）7.4%。 | [
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{
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{
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"entity": "溶血尿毒综合征",
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"label": "dis"
}
] |
然而，要注意到，反流性肾病是小儿终末期肾衰的重要原因之一，我院的资料表明，在小儿慢性肾功能不全的病因中，虽然获得性肾小球疾病仍占重要地位（占45.9%），但已与先天性和遗传性肾脏疾病平分秋色（占45.9%）。 | [
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其常见病因获得性肾小球疾病比例下降（66.7%→45.9%），先天性和遗传性肾脏疾病比例明显增加（33.3%→45.9%）。 | [
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结合20世纪70年代中期起的国外统计资料，也发现由获得性肾小球疾病引起的慢性肾功能不全逐渐减少，取而代之占主导地位的是先天性和遗传性肾脏疾病。 | [
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【发生机制】有关慢性肾衰竭的发病机制，历年来先后提出过“尿毒症毒素学说”、“矫枉失衡学说”、“肾小球高滤过学说”、“脂肪代谢紊乱学说”以及“肾小管高代谢学说”等等，晚近又有人提出“蛋白尿学说”、“慢性酸中毒学说”以及高蛋白饮食、肾内低氧对肾功能的影响等。 | [
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（一）健存肾单位的血流动力学改变肾单位受损或失用后，剩余健全的肾单位一系列适应性改变即负担起全肾功能性代偿及小球、小管各部分间的适应，部分健存肾单位功能高于正常，引起单个肾单位的肾小球滤过率增高，肾小球毛细血管压力增加，内皮细胞增生，系膜区基质增多，小球体积增大，逐步出现肾小球硬化。 | [
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{
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{
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"entity": "内皮细胞增生",
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"entity": "逐步出现肾小球硬化",
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] |
这一学说认为，CRF时体内某些物质的积聚，并非全部由于肾清除减少所致，而是机体为了纠正代谢失调的一种平衡适应，其结果又导致新的不平衡，如此周而复始，造成了进行性损害，成为CRF患者病情进展的重要原因之一。 | [
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] |
CRF时甲状旁腺素（parathyroidhormone，PTH）升高造成的危害是本学说最好的证据。 | [
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随着GRF降低，尿磷排泄量减少，引起高磷血症。 | [
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由于血清中钙磷乘积的升高，一方面使无机盐在各器官（包括肾脏）沉积，出现软组织钙化；另一方面，低钙血症又刺激了PTH的合成和分泌，代偿性促进尿磷排泄并升高血钙。 | [
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"entity": "血清",
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{
"id": 6,
"entity": "血钙",
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] |
但对甲状旁腺的持续性刺激则又导致甲状旁腺的增生及继发性甲状旁腺功能亢进（secondaryhyperparathyroidism，SHP），从而累及骨骼、心血管及造血系统等。 | [
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{
"id": 2,
"entity": "继发性甲状旁腺功能亢进",
"start_offset": 24,
"end_offset": 35,
"label": "dis"
},
{
"id": 3,
"entity": "secondaryhyperparathyroidism",
"start_offset": 36,
"end_offset": 64,
"label": "dis"
},
{
"id": 4,
"entity": "SHP",
"start_offset": 65,
"end_offset": 68,
"label": "dis"
},
{
"id": 5,
"entity": "骨骼",
"start_offset": 74,
"end_offset": 76,
"label": "bod"
},
{
"id": 6,
"entity": "心血管",
"start_offset": 77,
"end_offset": 80,
"label": "bod"
},
{
"id": 7,
"entity": "造血系统",
"start_offset": 81,
"end_offset": 85,
"label": "bod"
}
] |
矫枉失衡学说对于进一步解释各种慢性肾脏疾病进展的原因，加深人们对CRF时钙磷代谢紊乱及SHP发病机制的认识具有重要意义，因此一直为各国学者所推崇。 | [
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"entity": "慢性肾脏疾病",
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{
"id": 1,
"entity": "CRF",
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{
"id": 3,
"entity": "SHP",
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] |
首先，磷的潴留并非产生SHP的始动因素；只有当肾衰竭进入晚期（GFR＜20ml/min）时，患者才出现磷的潴留。 | [
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"entity": "磷的潴留",
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{
"id": 1,
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{
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"entity": "磷的潴留",
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] |
高磷血症不仅可以通过低钙血症，还可以通过其他途径直接或间接促进PTH的分泌。 | [
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"entity": "高磷血症",
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] |
磷对甲状旁腺还可能具有直接作用，因为低磷饮食可在血清中钙和1，25-（OH）2</sub>D3</sub>浓度无变化的情况下，降低PTH及其前体PTHmRNA的水平。 | [
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"id": 0,
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{
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{
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{
"id": 3,
"entity": "PTHmRNA",
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] |
其次，低钙血症也并非引起SHP的唯一直接原因。 | [
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除了低钙血症外，还有其他重要因素参与了SHP的形成。 | [
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现已证实SHP的发生和发展最重要的机制是：①1，25-（OH）2</sub>D3</sub>的缺乏和甲状旁腺对1，25-（OH）2</sub>D3</sub>的抵抗；②血钙水平对PTH分泌的调控作用减弱，即所谓调控点（set-point，指降低血清PTH水平至50%所需的钙离子浓度）上移，骨骼对PTH提高血钙的调节作用具有抵抗，加重了低钙血症；③肾脏对PTH的降解作用障碍，使血循环中残留的PTH片段增加等。 | [
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"id": 0,
"entity": "血钙",
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"id": 1,
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{
"id": 2,
"entity": "血清PTH",
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{
"id": 3,
"entity": "钙离子",
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{
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{
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{
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{
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"entity": "PTH",
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"label": "bod"
},
{
"id": 8,
"entity": "PTH",
"start_offset": 196,
"end_offset": 199,
"label": "bod"
}
] |
最近的研究表明口服补充生理剂量的1，25-（OH）2</sub>D3</sub>并不能完全抑制PTH的分泌，而仅仅在应用1，25-（OH）2</sub>D3</sub>冲击治疗导致体内超生理浓度时才能完全抑制PTH分泌，因此有学者提出甲状旁腺对1，25-（OH）2</sub>D3</sub>存在抵抗。 | [
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"entity": "生理剂",
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{
"id": 1,
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{
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{
"id": 4,
"entity": "甲状旁腺",
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"label": "bod"
}
] |
现已知甲状旁腺的主细胞中存在维生素D特异性受体（vitaminDreceptor，VDR），CRF时这种受体的密度和结合力均降低，使1，25-（OH）2</sub>D3</sub>作用下降。 | [
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"id": 0,
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{
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{
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{
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"entity": "vitaminDreceptor",
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{
"id": 5,
"entity": "CRF",
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] |
（三）尿毒症毒素目前已知的尿素、多胺类、胍类、中分子量物质及甲状旁腺素在尿毒症期血浓度都增高。 | [
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{
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{
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{
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{
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"entity": "血浓度",
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] |
它们对心脏、促红细胞生成素、Na-K-ATP酶、神经、肌肉以及血小板聚集代谢等均有一定毒性。 | [
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},
{
"id": 5,
"entity": "血小板",
"start_offset": 31,
"end_offset": 34,
"label": "bod"
}
] |
（四）肾小管间质损伤肾小管间质病变与肾小球疾病进展的关系已受到重视。 | [
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{
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{
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"entity": "肾小球疾病",
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] |
这种肾小管间质的形态学上的变化如肾小管萎缩、肾间质细胞浸润及间质纤维化一旦发生后，则进一步通过小管内阻力增加、正常的管球反馈功能丧失以及不能维持正常的渗透梯度等功能改变，加剧肾功能恶化。 | [
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{
"id": 1,
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{
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{
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},
{
"id": 5,
"entity": "管球",
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}
] |
（五）饮食影响膳食中高蛋白摄入可使入球小动脉扩张，加剧肾小球的高灌注损伤，并可加剧蛋白尿。 | [
{
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"entity": "膳食中高蛋白摄入可使入球小动脉扩张，加剧肾小球的高灌注损伤，并可加剧蛋白尿",
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] |
膳食中盐过高除影响全身血压外，观察到还可致肾小球容积加大和硬化，磷的摄入亦应限制，低磷饮食可防止钙磷盐沉积于血管壁和组织，抑制甲状旁腺的分泌。 | [
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{
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{
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"entity": "甲状旁腺",
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] |
高脂血症除影响内皮细胞外，还刺激肾小球系膜的增生及细胞外基质的积聚，而易发生肾小球硬化。 | [
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{
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] |
（六）肾素-血管紧张素系统（reninangiotensinsystem，RAS）在肾脏病进展中，血管紧张素Ⅱ（AⅡ）的作用也受到重视。 | [
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{
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{
"id": 2,
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] |
AⅡ可通过以下机制导致或加重肾脏病的进展：①作为一种血管活性物质，优先收缩肾小球出球小动脉刺激肾小球系膜的增生及细胞外基质的积聚，而易发生肾小球硬化系数；③促进水盐重吸收和兴奋肾交感神经；④作为促肾生长因子，除使系膜细胞增生肥大外，还能刺激其他血管活性物及细胞因子产生（如TGF-β1），导致细胞外基质进行性积聚；⑤抑制细胞外基质血管活性物质因引起肾小球高滤过而加重蛋白尿；⑦促进肾小管上皮细胞氨的产生，后者又通过激活补体引起肾损伤；⑧促进肾小管上皮细胞钠的重吸收，增加肾组织氧耗，引起肾组织氧供相对不足，加重肾损害。 | [
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{
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{
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{
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{
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{
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{
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"entity": "细胞",
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{
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},
{
"id": 11,
"entity": "肾小球",
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},
{
"id": 12,
"entity": "蛋白尿",
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"label": "bod"
},
{
"id": 13,
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"label": "bod"
},
{
"id": 14,
"entity": "肾小管上皮细胞",
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}
] |
【临床表现】（一）电解质、酸碱代谢失常1.水代谢早期由于浓缩功能减退，尿量不减少或反而增多，晚期尿量才有减少，终末期可发展到无尿。 | [
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{
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"entity": "终末期可发展到无尿",
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] |
患者对水代谢调节能力减退，当水分摄入过多时，易在体内潴留并形成稀释性低钠血症，摄入过少时也易引起体内水分不足。 | [
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{
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{
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"entity": "摄入过少时也易引起体内水分不足",
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] |
2.钾代谢有高钾血症趋势，细胞内钾的积聚与Na-KATP酶活力下降有关。 | [
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{
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] |
高钾血症可随外伤、手术、麻醉、输血、酸中毒及突然更改饮食等而加剧，慢性肾衰时血钾升高是一方面，但总体钾的存储量仍降低，所以保持钾的正常平衡仍是潴留。 | [
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"entity": "高钾血症",
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{
"id": 1,
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{
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{
"id": 3,
"entity": "血钾",
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"label": "ite"
},
{
"id": 4,
"entity": "总体钾的存储量仍降低，所以保持钾的正常平衡",
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},
{
"id": 5,
"entity": "潴留",
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"label": "dis"
}
] |
3.钠代谢CRF可以维持钠正常平衡状态相当长时间，这与健存肾单位及利钠激素等体液因子有关。 | [
{
"id": 0,
"entity": "CRF",
"start_offset": 5,
"end_offset": 8,
"label": "dis"
},
{
"id": 1,
"entity": "利钠激素",
"start_offset": 33,
"end_offset": 37,
"label": "bod"
},
{
"id": 2,
"entity": "体液因子",
"start_offset": 38,
"end_offset": 42,
"label": "bod"
}
] |
（1）钠消耗型：盐分丢失型肾病因细胞外液的缩小及低血压等均有钠酸中毒失。 | [
{
"id": 0,
"entity": "盐分丢失型肾病",
"start_offset": 8,
"end_offset": 15,
"label": "bod"
},
{
"id": 1,
"entity": "酸中毒",
"start_offset": 31,
"end_offset": 34,
"label": "dis"
}
] |
很多疾病可引起盐分丢失，如肾盂肾炎、肾髓质囊性病、肾积水及间质性肾炎等，这类病人的集合管往往不能吸收运输过来足够量的钠盐而出现低钠。 | [
{
"id": 0,
"entity": "肾盂肾炎",
"start_offset": 13,
"end_offset": 17,
"label": "dis"
},
{
"id": 1,
"entity": "肾髓质囊性病",
"start_offset": 18,
"end_offset": 24,
"label": "dis"
},
{
"id": 2,
"entity": "肾积水及间质性肾炎",
"start_offset": 25,
"end_offset": 34,
"label": "dis"
}
] |
（2）钠潴留型：当摄入钠过多时，不能正常排泄以致钠潴留，体内细胞外容量增加，发生高血压、肺充血与心脏扩大，甚至心力衰竭。 | [
{
"id": 0,
"entity": "当摄入钠过多时，不能正常排泄以致钠潴留，体内细胞外容量增加，发生高血压、肺充血与心脏扩大，甚至心力衰竭",
"start_offset": 8,
"end_offset": 59,
"label": "sym"
}
] |
4.酸碱平衡慢性肾衰病人早期肾小管合成氨的肾盂肾炎力未全丧失，可动员体内其他缓冲系统来代偿代谢性酸中毒，如呼吸系统，组织代偿如骨盐的丢失等。 | [
{
"id": 0,
"entity": "肾小管",
"start_offset": 14,
"end_offset": 17,
"label": "bod"
},
{
"id": 1,
"entity": "肾盂肾炎",
"start_offset": 21,
"end_offset": 25,
"label": "dis"
},
{
"id": 2,
"entity": "呼吸系统",
"start_offset": 53,
"end_offset": 57,
"label": "bod"
}
] |
当病情进展，健存肾单位进一步减少，GFR＜20ml/min时肾脏排泄有机酸能力下降，排氨能力减低，引起酸中毒肺充血血pH＜7.25时要警惕合并酮症酸中毒。 | [
{
"id": 0,
"entity": "当病情进展，健存肾单位进一步减少，GFR＜20ml/min时肾脏排泄有机酸能力下降，排氨能力减低",
"start_offset": 0,
"end_offset": 48,
"label": "sym"
},
{
"id": 1,
"entity": "引起酸中毒肺充血血pH＜7.25时要警惕合并酮症酸中毒",
"start_offset": 49,
"end_offset": 76,
"label": "sym"
}
] |
5.其他电解质慢性肾衰病人不能充分排泄氯离子，高氯血症与钠浓度成正比；血钙浓度往往降低，慢性肾衰患者常能忍受低血钙而不致搐搦，这些患者的肠道钙的吸收能力下降，口服活性维生素D可提高血钙浓度；当GFR＜20ml/min时，血镁可升高，尿血pH减少。 | [
{
"id": 0,
"entity": "慢性肾衰病",
"start_offset": 7,
"end_offset": 12,
"label": "dis"
},
{
"id": 1,
"entity": "高氯血症",
"start_offset": 23,
"end_offset": 27,
"label": "dis"
},
{
"id": 2,
"entity": "钠浓度",
"start_offset": 28,
"end_offset": 31,
"label": "ite"
},
{
"id": 3,
"entity": "血钙",
"start_offset": 35,
"end_offset": 37,
"label": "ite"
},
{
"id": 4,
"entity": "慢性肾衰",
"start_offset": 44,
"end_offset": 48,
"label": "dis"
},
{
"id": 5,
"entity": "血钙",
"start_offset": 55,
"end_offset": 57,
"label": "ite"
},
{
"id": 6,
"entity": "活性维生素D",
"start_offset": 81,
"end_offset": 87,
"label": "dru"
},
{
"id": 7,
"entity": "血钙",
"start_offset": 90,
"end_offset": 92,
"label": "ite"
},
{
"id": 8,
"entity": "血镁",
"start_offset": 110,
"end_offset": 112,
"label": "ite"
},
{
"id": 9,
"entity": "血pH",
"start_offset": 117,
"end_offset": 120,
"label": "ite"
}
] |
当血镁较高（＞2mmol/L）有临床症状时则可应用排钠利尿剂，促镁排出，纠正脱水，必要时给透析疗法。 | [
{
"id": 0,
"entity": "血镁",
"start_offset": 1,
"end_offset": 3,
"label": "ite"
},
{
"id": 1,
"entity": "排钠利尿剂",
"start_offset": 25,
"end_offset": 30,
"label": "dru"
},
{
"id": 2,
"entity": "透析疗法",
"start_offset": 45,
"end_offset": 49,
"label": "pro"
}
] |
GFR＜20ml搐搦min时，血磷升高较明显，病情进展到肾脏排磷进一步减少。 | [
{
"id": 0,
"entity": "搐搦",
"start_offset": 8,
"end_offset": 10,
"label": "dis"
},
{
"id": 1,
"entity": "血磷",
"start_offset": 15,
"end_offset": 17,
"label": "ite"
}
] |
（二）血管系统1.高血压常见原因有①GFR下降、NO分泌减少，使VDML血管减低的髓脂质下降，引起细胞外容量增加，心搏出量增加，继而外周阻力增加，血排钠利尿剂②肾素、血管紧张素及醛固酮系统活跃，肾素分泌过多。 | [
{
"id": 0,
"entity": "高血压",
"start_offset": 9,
"end_offset": 12,
"label": "dis"
},
{
"id": 1,
"entity": "排钠利尿剂",
"start_offset": 74,
"end_offset": 79,
"label": "dru"
}
] |
2.心包炎尿毒性心包炎似由不明的生化物质、尿酸沉积及代谢异常所引起。 | [
{
"id": 0,
"entity": "尿毒性心包炎",
"start_offset": 5,
"end_offset": 11,
"label": "dis"
}
] |
属纤维性心包炎，有渗出、出血，可闻及心包摩擦音，偶发生心包填塞VDML血管减低的髓脂质下降，有不同程度的心肌肥厚，间质纤维化，心肌钙化，草酸盐沉积。 | [
{
"id": 0,
"entity": "纤维性心包炎",
"start_offset": 1,
"end_offset": 7,
"label": "dis"
},
{
"id": 1,
"entity": "有渗出、出血，可闻及心包摩擦音",
"start_offset": 8,
"end_offset": 23,
"label": "sym"
},
{
"id": 2,
"entity": "VDML血管减低的髓脂质下降",
"start_offset": 31,
"end_offset": 45,
"label": "sym"
},
{
"id": 3,
"entity": "有不同程度的心肌肥厚",
"start_offset": 46,
"end_offset": 56,
"label": "sym"
},
{
"id": 4,
"entity": "间质纤维化，心肌钙化，草酸盐沉积",
"start_offset": 57,
"end_offset": 73,
"label": "sym"
}
] |
临床表现心脏扩大，心输出量减少，各种心律失肾素。 | [
{
"id": 0,
"entity": "心脏扩大，心输出量减少",
"start_offset": 4,
"end_offset": 15,
"label": "sym"
},
{
"id": 1,
"entity": "各种心律失肾素",
"start_offset": 16,
"end_offset": 23,
"label": "sym"
}
] |
（三）胃肠系统胃纳减退，常见有呕吐及恶心等症状，加重了水、盐代谢及酸碱平衡紊乱，负氮平衡加剧，对钙的吸收下降。 | [
{
"id": 0,
"entity": "胃纳减退，常见有呕吐及恶心等症状，加重了水、盐代谢及酸碱平衡紊乱，负氮平衡加剧，对钙的吸收下降",
"start_offset": 7,
"end_offset": 54,
"label": "sym"
}
] |
另外消化道出血偶发生心包填塞于黏膜有弥散性小出血点炎症及溃疡引起。 | [
{
"id": 0,
"entity": "偶发生心包填塞",
"start_offset": 7,
"end_offset": 14,
"label": "sym"
},
{
"id": 1,
"entity": "黏膜有弥散性小出血点炎症及溃疡引起",
"start_offset": 15,
"end_offset": 32,
"label": "sym"
}
] |
（四）精神神经症状，乏力、失眠、激惹、压抑、记忆力减退或反抗心理行为尿毒症伴有各种心律失常能亢进时可使脑细胞钙离子浓度增高，出现不正常脑电图。 | [
{
"id": 0,
"entity": "精神神经症状，乏力、失眠、激惹、压抑、记忆力减退或反抗心理行为",
"start_offset": 3,
"end_offset": 34,
"label": "sym"
},
{
"id": 1,
"entity": "尿毒症",
"start_offset": 34,
"end_offset": 37,
"label": "dis"
},
{
"id": 2,
"entity": "各种心律失常",
"start_offset": 39,
"end_offset": 45,
"label": "sym"
},
{
"id": 3,
"entity": "脑细胞钙离子浓度",
"start_offset": 51,
"end_offset": 59,
"label": "ite"
},
{
"id": 4,
"entity": "脑电图",
"start_offset": 67,
"end_offset": 70,
"label": "ite"
}
] |
临床可有谵妄、木僵，甚至昏迷。 | [
{
"id": 0,
"entity": "谵妄、木僵，甚至昏迷",
"start_offset": 4,
"end_offset": 14,
"label": "sym"
}
] |
周围神经症状如痛性肢体麻痹，深腱反射消失，消化道出血、痉挛甚至感觉消失，被认为与体内中分子物质积聚有关。 | [
{
"id": 0,
"entity": "周围神经症状如痛性肢体麻痹，深腱反射消失",
"start_offset": 0,
"end_offset": 20,
"label": "sym"
},
{
"id": 1,
"entity": "消化道出血",
"start_offset": 21,
"end_offset": 26,
"label": "sym"
},
{
"id": 2,
"entity": "痉挛甚至感觉消失",
"start_offset": 27,
"end_offset": 35,
"label": "sym"
}
] |
（五）血液系统1.贫血呈正血色素、正细胞性记忆力减退随肾功能减退而加剧。 | [
{
"id": 0,
"entity": "贫血",
"start_offset": 9,
"end_offset": 11,
"label": "sym"
},
{
"id": 1,
"entity": "呈正血色素、正细胞性记忆力减退随肾功能减退而加剧",
"start_offset": 11,
"end_offset": 35,
"label": "sym"
}
] |
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