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动脉粥样硬化和高血压

2018-09-26 76页 ppt 9MB 11阅读

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动脉粥样硬化和高血压胡某男50岁连云港市人2004年4月19初诊,10月前突感胸闷,胸痛,憋气,怵惕,惊悸,无力,畏寒,下肢凉TCG:T波广泛低平,血压170/150.脉沉而拘紧,舌尚可。证:寒闭心脉方:小青龙汤药:麻黄桂枝细辛炮附子干姜半夏白芍五味子茯苓红参炙甘草病例①氧化LDL→oxLDL。②吞噬oxLDL→泡沫细胞。③坏死→释放脂质→细胞外脂质池④释放溶酶体酶→损伤内皮细胞、SMC和M。⑤产生细胞因子→VEC表达黏附分子→PMN、M、Pt黏附。↘SMC迁移、增殖。⑥激活T...
动脉粥样硬化和高血压
胡某男50岁连云港市人2004年4月19初诊,10月前突感胸闷,胸痛,憋气,怵惕,惊悸,无力,畏寒,下肢凉TCG:T波广泛低平,血压170/150.脉沉而拘紧,舌尚可。证:寒闭心脉方:小青龙汤药:麻黄桂枝细辛炮附子干姜半夏白芍五味子茯苓红参炙甘草病例①氧化LDL→oxLDL。②吞噬oxLDL→泡沫细胞。③坏死→释放脂质→细胞外脂质池④释放溶酶体酶→损伤内皮细胞、SMC和M。⑤产生细胞因子→VEC达黏附分子→PMN、M、Pt黏附。↘SMC迁移、增殖。⑥激活T淋巴细胞→淋巴因子→和细胞因子诱导SMC凋亡。⑦释放溶酶体酶、蛋白水解酶和自由基→破坏纤维帽→斑块不稳定。*Atheroscleroticplaquehas2maincomponents:asoft,lipid-richcoreandahard,collagen-richfibrouscap.Instableplaques,athickfibrouscapmayrepresent>70%ofplaquevolume.Itstabilizestheplaqueandpreventsitfromundergoingrupture.Incontrast,unstableplaquehasathinfibrouscapandisatgreaterriskforrupture.Inunstableplaque,thelipid-richcoremayrepresentthemajorityoftheplaquevolume.Thecoreisrichinextracellularlipids,whichareformedbytrappingblood-derivedlipids,notablylow-densitylipoprotein,orbylipid-filledmacrophages,knownasfoamcells.Theplaquedestabilizesduetoinflammationbyfoamcellsandotherinflammatorymediatorsthatmaketheplaquemorevulnerabletorupture.Thiscommonlyoccursatthejunctionoftheplaqueandthelessdiseasedvesselwall.Asaresult,thelipidcoremaybeexposedtoflowingbloodleadingtoplatelet-mediatedthrombusformation.FalkreviewedtheworkofotherinvestigatorsregardingtheseverityofstenosisanditsassociationwiththeriskofMI.Resultsshowedthat>86%ofMIsresultedfromlesionsthatwere<70%stenosed.MostexpertspriortoFalkthoughtthatpatientshadheartattacksbecauseofblockagesthatincreasedinsizeuntiltheyblockedthebloodvesselandcausedaheartattack.1BasedonthefindingsofFalk,wenowknowtheprimarycauseofaheartattackistheruptureofunstableplaquesthatare<70%stenosedandareclinicallysilent.Approximately200patientsfrom4studieswerestudiedtogeneratetheseresults,whichhavebeenconfirmedinotherstudies.1References1FalkE,ShahPK,FusterV.Coronaryplaquedisruption.Circulation.1995;92:657-671.2LibbyP.Molecularbasesoftheacutecoronarysyndromes.Circulation.1995;91:2844-2850.冠状动脉主动脉脑动脉肾动脉肠系膜动脉四肢动脉(三)脑动脉粥样硬化脑缺血、脑萎缩、”脑卒中”(四)其他肾动脉粥样硬化缺血性肾病、肾性高血压肠系膜动脉粥样硬化肠缺血、肠坏死四肢动脉粥样硬化下肢运动障碍、足坏疽胡某男50岁连云港市人2004年4月19初诊,10月前突感胸闷,胸痛,憋气,怵惕,惊悸,无力,畏寒,下肢凉TCG:T波广泛低平,血压170/150.脉沉而拘紧,舌尚可。证:寒闭心脉方:小青龙汤药:麻黄桂枝细辛炮附子干姜半夏白芍五味子茯苓红参炙甘草病例第二节高血压hypertension1.功能紊乱期2.动脉病变期3.内脏病变期良性高血压分期细,小动脉间歇性痉挛各器官无器质性变化功能紊乱期1.细动脉硬化:细动脉壁玻璃样变性(高血压主要病变特征)2.小动脉硬化:管壁增厚变硬,管腔狭窄。3.大动脉,中等动脉硬化:管壁增厚变硬,管腔扩张弯曲,常伴发动脉症状:头痛,眩晕,疲乏,注意力不集中,续压持续升高。动脉病变期1.心脏左心室代偿性肥大冠状动脉硬化心力衰竭内脏病变期2.肾脏:肾小球纤维化与玻璃样变。肾小管萎缩消失。肾脏体积缩小,质地变硬,重量减轻肾功能不全3.脑:高血压脑病:头痛眩晕,呕吐,视力模糊,意识障碍等脑软化脑出血内脏病变期内脏病变期视网膜病变:视网膜水肿,有渗出物与出血,影响视力。特征:好发于年轻人,血压急剧升高,达130以上。病理变化:全身细动脉壁广泛性血浆浸润,纤维样坏死,红细胞露出,管壁厚度增加,甚至引发梗死。恶性高血压3.社会心理应激因素发达国家高于发展中国家改变体内激素平衡城市居民高于农村经常遭受生活事件刺激者高血压发病的1.精神神经源学说:精神刺激,血管舒缩中枢形成兴奋灶,交感神经兴奋。2.肾源学说:肾小管旁器刺激,血管紧张素形成并发挥作用。3.摄钠过多学说4.细小动脉重构肝肾阴虚,肝阳上亢。高血压中医病机*Atheroscleroticplaquehas2maincomponents:asoft,lipid-richcoreandahard,collagen-richfibrouscap.Instableplaques,athickfibrouscapmayrepresent>70%ofplaquevolume.Itstabilizestheplaqueandpreventsitfromundergoingrupture.Incontrast,unstableplaquehasathinfibrouscapandisatgreaterriskforrupture.Inunstableplaque,thelipid-richcoremayrepresentthemajorityoftheplaquevolume.Thecoreisrichinextracellularlipids,whichareformedbytrappingblood-derivedlipids,notablylow-densitylipoprotein,orbylipid-filledmacrophages,knownasfoamcells.Theplaquedestabilizesduetoinflammationbyfoamcellsandotherinflammatorymediatorsthatmaketheplaquemorevulnerabletorupture.Thiscommonlyoccursatthejunctionoftheplaqueandthelessdiseasedvesselwall.Asaresult,thelipidcoremaybeexposedtoflowingbloodleadingtoplatelet-mediatedthrombusformation.FalkreviewedtheworkofotherinvestigatorsregardingtheseverityofstenosisanditsassociationwiththeriskofMI.Resultsshowedthat>86%ofMIsresultedfromlesionsthatwere<70%stenosed.MostexpertspriortoFalkthoughtthatpatientshadheartattacksbecauseofblockagesthatincreasedinsizeuntiltheyblockedthebloodvesselandcausedaheartattack.1BasedonthefindingsofFalk,wenowknowtheprimarycauseofaheartattackistheruptureofunstableplaquesthatare<70%stenosedandareclinicallysilent.Approximately200patientsfrom4studieswerestudiedtogeneratetheseresults,whichhavebeenconfirmedinotherstudies.1References1FalkE,ShahPK,FusterV.Coronaryplaquedisruption.Circulation.1995;92:657-671.2LibbyP.Molecularbasesoftheacutecoronarysyndromes.Circulation.1995;91:2844-2850.
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