病理生理学("thophysiology):是一门研究疾病发生，发展，转归的规律和机制的科学，其重点研究疾病中功能和代谢变化病理过程MtholowicM process):是指多种疾病过程中可能出现的共同的\成套的功能代谢和形态结构的病理变化.疾病发生的条件(DredisDosii吃factor):主要是指那些能够影响疾病发生的各种机体内外因素疾病(disease):疾病是机体在一泄条件下.由病因与机体相互作用而产生的一个损伤与抗损伤斗争的有规律过程，临床出现许多不同的症状与体征，机体与外环境间的协调发生障碍・Disease is referred asan aberrant manifestation of homeostatic disturbances caused by harmful agents・病因(cause):又称原因，是引起某种疾病的因素，又决左该疾病的特异性，是疾病发生必不可缺少的因素. Causative factor or pathogenic cause is referred as the factor that can cause a disease and determine its specificity・诱因（percipitatin父factoid•能加强病因作用或促进疾病发生的因素完全康复:指疾病时所发生的损伤性变化完全消失不完全康复:疾病是的损伤性变化得到控制•但基本病理变化尚未完全消失，经机体代偿后功能代谢恢复,主要症状消失，有时可留后遗症脑死亡(brain death):—般均已枕大孔以上全脑死亡作为脑死亡标准.Brain death is a state of permanent irreversible cessation of whole brain activity・低容虽性髙钠血症(hypovolemic hypernatremia, hypertonic dehydration )又称髙渗性脱水,其特征细胞内液和细胞外液均减少，是失水多于失钠，血淸钠浓度>150ml/L,血浆渗透压>310mmol/L.低容量性低钠血症(hypovolemic hyponatremia, hypotonic dehydration)又称低渗性脱水,其特征是失钠多于失水,细胞外液渗透压低于280mmol/L,血淸钠浓度低于130mmol/L.等渗性脱水(isotonic dehydEion)是指机体的水和钠以等渗比例丢失，或失液后经机体调i'j血浆渗透压仍在正常范風血淸钠浓度为130-150mmol/L,>浆渗透压为280-310 mmol/L.水中毒(water intoxication):髙容量性低钠I血症•机体的排水能力降低,导致低渗性液体在体内潴留，使细胞内\外液都增多，引起重要器官功能障碍.特点:血淸Na+ <130mmol/L.I(IL浆渗透压<280mmol/L.患者有水潴留,使体液疑明显增多.水肿(edem初:过多体液在组织间隙或体腔内积聚称为水肿冰肿发生于体腔，称为枳水Edema means that excessive fluid accumulates in interstitial compartment and some cavities in the body・反常性酸性尿:一般碱中毒时尿液呈碱性，但在低K+血症性碱中毒时細胞内K+外移\H+进入细胞致细胞外液緘中毒，肾小管上皮细胞H+增多\泌H+增加\使尿液反常性地呈酸性.反常性碱性尿高血钾性酸中毒时K+进入肾小管上皮细胞\细胞内H+外移\肾小管上皮细胞H十减少\泌H+减少\使尿液反常性地呈碱性.代谢性酸中毒(metabolic acidosis):由于细胞外液H增加或HCO3丢失而引起血浆HCO3-原发性减少所引起的pH值降低.AB.SB.BB降低.BE负值加大,PH下降,通过呼吸代偿,PaCO2继发性下降,AB<SB 呼吸性酸中毒(respinitoc acidosis)：由于二氧化碳代谢障碍或吸入过多而引起以血浆碳酸浓度升髙. PH降低.PaCO2增高.AB.SB.BB升髙,AB>SB,BE正值增大代谢性碱中毒(metabolic MkMosis):由于细胞外液碱增多或H丢失而引起血浆HCO3-原发性增高所引起的pH值升高.PH升髙.AB.SB.BB升高,BE正值增大.AB>SB呼吸性碱中毒(respiratory alkalosis):由于肺通气过度引起的血浆碳酸浓度原发性减少pH值升髙.Pa CO2降低,PH升髙.ABvSB•代偿后代谢性指标继发性降低‘AB.SB.BB降低・BE负值加大垦标准碳酸氢盐•标准条件下测得的血浆HCO3-浓度(38 C Hb完全氧合PCO2 =40mmHg)・正常：2 2-27 mmol/L(24 mmol/L)反映代谢因素連：实际碳酸氢盐•概念：实际条件下测得的血浆HCO3-浓度.正常人：AB=SB堕:缓冲碱:血液中一切具有缓冲作用的阴离子总量•正常值：45-52 mmol/L (48 mmol/L).意义：反映代谢因素•原发性一代酸,原发性一代碱碱剩余:BE:标准条件下，将1升全或血浆滴左到pH 7.4所需的酸或緘的量•正常值：0±3 mmol/L. Sk：反映代谢因素:BE正值增大一代碱.BE负值增大一代酸址:阴离子间隙•血Na+浓度减去血C1 一和HCO3 —的浓度,等于血浆中未测定阴离子(UA)与未测左阳离子(UC)的差值.意义：反映血浆固左酸含量\区分代酸的类型和混合型酸碱平衡紊乱.正常范国10〜1 4mmol/L( ＞16mmol/L 为界限)it's the deference between the concentrations of unmeasured a nion(UA) and unmeasured cation(UC) in plasma (AG=UA-UC). The AG value can be obt ained by calculating the difference between plasma concentration of major measured cat ion (Na) and the sum of the plasma concentrations of major measured anions (Cl and HCO3), that is, AG = [Na+] - ([Cl] + [HCO3]). Its normal range is 12+-2 mmol/L缺氧(HwoxinanoxiM凡因组织供氧不足或用氧障碍.使组织和细胞的代谢\功能甚至形态结构发生异常的病理过程.Hypoxia can be defined as a deficiency in either oxygen delivery or its ut ilization at the tissue level or the deficiency of both, which can lead to changes in fun ction, metabolism and even structure of the body低张性缺氧(hypotonic hypoxia):也称为乏氧性缺氧(hypoxic hypoxia)由于吸入气中氧分压降低或外呼吸功能障碍所致的缺氧,一动脉血氧分血液性缺氧(hemic hypoxin):又称为等张性低氧血症(isotonic hypoxia).由于ifll.红蛋白数量减少或性质改变,以致血氧含量降低或血红蛋白结合的氧不易释岀所引起的缺氧Hemic hypoxia refers to hyp oxia resulting from a low carrying capacity of oxygen in the blood caused by an altere d affinity of Hb for oxygen or a decrease in the amount of Hb in the blood・循环性缺氧:由于心输出虽:减少，组织灌流量减少或静脉淤血』IL流速度减慢所引起的缺氧，又称为低动力性缺氧(hypkinetic hypoxia)组织性缺氧:由于组织细胞利用氧障碍所引起的缺氧,又称为组织中毎性缺氧(dysoxidalivc hypoxia ) 紫组(cvanosis):毛细血管内脱氧血红蛋白平均浓度增加到5g/dl以上，可使皮肤与粘膜呈青紫色，称为发纟甘.Cyanosis refers to the violaceous color of skin and mucous membranes which occurs as the deoxyhemoglobin concentration of the blood in capillaries becomes greater than 5g/dl.肠源性青紫(enterogenous cyanosis):引进使导致大量血红蛋白氧化而导致髙铁血红蛋白血症When p ickled vegetables containing nitrate are consumed in large amounts, the reabsorbed nitra te reacts with HbFe2* to form HbFe u OH・ The color of skin becomes coffee color. Thi s phenomenon is called enterogenous cyanosis・发热(feve门:由于致热原的作用使体温调立点上移.而引起的调肖性体温升髙(超过0.5C).体温旦调定点, 主动性(调控下)有热限(S41°C )，致热细胞因子:神经-内分泌-免疫Fever is a complicated patholog ical process characterized by a regulated elevation of core body temperature, in which t he hypothalamic set point is temporarily reset at an elevated temperature in response to pyretic substances过热(hgerthemhi):调立点并未发生移动.而是由于体温调肖障碍或散热障碍及产热器官功能异常等. 体温调肖机构不能降体温控制在与调左点相适应的水平上，调定点正常，体温＞调定点，被动性(失控)，无热限(可＞41 °C )内生致热原(endogenous EP):产内生致热原细胞在发热激活物的作用下.产生和释放的能引起体温升髙的物质.Endogenous pyrogens are described as cytokines inducing fever, which are produced and released by EP cells, such as interleukin-1, tumor necrosis factor, etc.细胞凋亡(cell apoMosis):由体内外因素触发细胞内预存的死亡程序而导致的细胞死亡过程.it's a cel luar suicide route that allows for the selective removal of superfluous and potentially d angerous cells as well as for tissue remoding and homeostasis凋上小体(apoptosis body):细胞发生凋亡时因细胞膜皱缩内陷扮割包裹胞浆所形成的泡状小依凋亡细胞特征性的形态学改变Stress:机体受到内外环境因素及社会心理因素刺激时所出现非特异性全身性反应称为stress或应激反应(stress responsejit^ defined as a systemic nonspecific response ofthe body to environ mental demands or pressures made upon it Stressor:应激原，包含:外环境因素，内环境因素，心理会环境因素The stimulus that provokes a stress response is referred to as stressor全身适应综合征(general adaMion svndrome):对大务数的应激反应，在撤除应激原后，机体可很快趋于平静.恢复自稳态.但如果劣性应激原持续作用于机体，则应激可表现为一个动态的连续过程，并最终导致内环境紊乱和疾病，称之为全身适应综合征急性期反应(acute phase response, APR):感染，烧伤，大手术，创伤等应激原可诱发机体产生快速反应,如体温升高，血糖升高,分解代谢增强，负氮平衡及血浆中某些蛋白质浓度迅速变化等热休克蛋白(HSP):应激反应时细胞新合成或合成增加的一类髙度保守的蛋白质，在细胞内发挥作用，属非分泌型蛋白・A family of stress proteins which are induced in cells exposed to heat stre ss or other stressors Its funcetions mainly as a molecular chaperones to help the new p eptide chain in folding and translocation and reponring the injured protein应激性溃疡(stress ulcer):病人在遭受各类重伤\重病和英它应激情况下.出现胃\十二指肠粘膜的急性病变，主要表现为胃\十二肠粘膜的糜烂\浅溃疡\渗血等,少数可较深或穿孔.急性期反应蛋白(acute phase i)n)feii】、APP):应激时由于炎症\感染或组织损伤等原因可使血浆中某些蛋白质的浓度迅速变化，并在血浆中迅速改变含量的蛋白质.缺血•再灌注损伤(ischemimreperfusion iniurv):任一立条件下缺血后恢复血流环仅不能使组织器官功能恢复，反而使组织器官损伤加重甚至发生不可逆性损伤的现象.The restoration of blood flow af ter transient ischemia may be associated with further reversible or irreversible cell dama ge, which is called ischemia-reperfusion injury or reperfusion injury.聶超载(calcium overload)：细胞内钙过量积聚.引起组织器官功能及结构损伤•称为钙超载或钙超负荷.Calcium overload refers to that intracellulai* content of calcium is increased abnormally during ischemia and reperfusion, which results in the disorder of cellular structure and function 氧反专(augen mzdox):用低氧或无氧液培养细胞一段时间后恢复正常氧供.细胞损伤更趋严重.钙反常(calcium ”radox):预先用无钙溶液短暂灌流后.恢复正常含钙溶液灌流.导致细胞外Ca2+大量内流而引起细胞损伤进一步加重的现象.Dh反常(PH paradox):再灌注时迅速纠正缺血组织的酸中毒，损伤反而进一步加重的现象些藝:再灌注期组织获得氧的供应，激活的中性粒细胞耗氧增加.产生大量的氧自由基造成细胞损伤，称为呼吸爆发(respiratory burst)/氧爆发(oxygen burst).无复流现象(no・reflow phenomenon):在结扎动脉造成局部缺血后，再打开结扎的动脉，缺血区并无血液灌注，称谓无复流现象.休克(shock):多病因，多发病环节，多钟体液因子参与，微循环混乱，全身有效循环血不足，可导致多器官功能障碍，全身调节性紊乱.Shock is a pathological process caused by various drastic etiologic al factors, which is characterized by microcirculation failure resulting from decreased ef fective circulatory blood volume and inadequate tissue perfusion with the results of cell ular metabolism impediment and dysfunction of multiple vital organ 自身输血(Auto blood transfusion) At the early stage of shock, vessel constriction because of release of a large amount of vasoconstrictors may mobilize the stored blood to parti cipate in the circulation, which is considered as compensation of venous return.自身输液(Auto fluid transfusion)At the early stage of shock, significant decrease of hydros tatic pressure in capillary may drive fluid to shift from interstitial space to the vascular compartment, and as a result, the plasma volume can be partly restored as a compens atory response缺血性缺氧(Ischemic hypoxia)The deficiency of blood perfusion to tissues caused by decre asedarterial pressure or obstruction of arteries is called ischemic hypoxia.心源性休克(cardiogenic shock):大而积心肌梗死\急性心肌炎\心脏压塞及严重的心律紊乱而引起心输出量锐减导致的休克称心源性休克.低血容量性休克(hvpoYolemic shock)：由于血蚩:减少引起的休克，见于失血、失液或饶伤等情况. 感染性休克:严重感染特别是格兰阴性菌感染常可引起•又称脓毒性休克,指有微生物及其毒素等产物引起的脓毒病综合征伴休克.多系统器官衰竭(\IOF):在严重创伤\感染\休克或复苏后，短期内出现两个或两个以上系统\器官衰竭. 炎症瀑布反应(infkimm玳OH zszde):炎细胞激活产生的多种促炎细胞因子可导致炎症细胞活化.两者互为因果.全身炎症反应综合征(SIRS)：机体失控的自我持续放大和自我破坏的炎症，表现为播散性炎症细胞活化和炎症介质泛滥到血浆并在远隔部位引起全身性炎症.It's defined as in severe injury or compli cated with infection,the host inflammatory response may persist inappropriately leading t o systemic inflammatoiy response syndrome it's an important element leading to MODS 代偿性抗炎反应综合征(CARS):指感染或创伤时机体产生可引起免疫功能降低和对感染易感性增加的或与强烈的内源性抗炎反应内源性抗炎反应.An endogenous anti-inflammatory response wit h impaired immune function and infestious predisposition caused by excess release of a nti-inflammatory mediators多器官功能障码矗合征(MODS ):在严重创伤,感染和休克时，原无器官功能障碍的患者同时或在短时间内相继出现两个以上器官系统的功能障碍以致机体内环境的稳左必须靠临床「预才能维持的综合症.it's refers to dysfunctions of more than two organs occur successively in patients wit hout pre-exit dysfunction 盛:弥散性血管内凝血.致病因子作用下，凝血因子和血小板被激活，大量促凝物质入血，凝血酶增加，微循环中广泛性微血栓形成,使凝血因子和血小板被消耗，继发性纤维蛋白溶解功能增强,导致患者出血\ 休克\器官功能障碍和溶血性贫等临床表现的危重临床综合征DIC is a pathological process caus ed by disturbance of the kinetic balance between coagulation and anticoagulation system s (including fibrinolytic system). Etiologic factors activate extensive intravascular coagul ation and secondary fibrinolysis. The clinical features of DIC are bleeding, shock, orga n dysfunction and microangiopathic hemolytic anemia微血管病性溶血性岔血(microangioD玳hie hemolvtic anemia):待征是外周血图片中可见一些特殊形态各异的变形红细胞，称为裂体细胞裂体细胞(schistocvte):在DIC岀现的溶血性贫血中，外周血涂片中出现一些形态特殊的变形红细胞，苴外形呈盔甲形\新月形\星形等，统称这些变形的红细胞为裂体细胞.“3P”试验(鱼精蛋白副凝试验):主要监测血浆中FDP的X片断，鱼精蛋白入血浆一鱼精蛋白与FDP结合一使FDP与纤维蛋白单体分离，纤维蛋白单体彼此聚合凝固形成白色沉淀，不需酶而形成纤维蛋白的现彖称副凝试验.DIC者呈阳性心力衰竭(heart fidkire):在并种致病因素的作用下心脏的收缩和(或)舒张功能发生障碍.使心输出量绝对或相对下降，以致不能满足机体代谢需要的病理过程或综合征.It's a pathological process in wh ich the systolic or/ and diastolic function of the heart is impaired, and as a result, card iac output decreases and is unable to meet the metabolic demands of the body.心肌向心性肥大(concentric hypertrophy):在长期过度的压力负荷作用下.心肌纤维呈并联性增生.肌纤维变粗，心室壁厚度增加，心腔无明显扩大，室腔直径与室壁厚度的比值小于正常.心肌离心性肥大(eccentric hypertrophy):在长期过度的容量负荷作用下.心肌纤维呈串联性增生.肌纤维长度增加，心腔明显扩大，室腔直径与室壁厚度的比值等于或大于正常.高输出量性心力衰竭(hi父h output heart failure)严重贫血.妊娠，甲亢.动静脉痿及VB1缺乏时，因血容量扩大或循环速度加快,静脉回流增加，心脏过度充盈,代偿阶段期心排出量明显髙于正常，处于高动力循环状态，心衰发生时心输出量较发病前有所下降，但其值仍属正常,甚至高于正常.It indicates that t he cardiac output may be supra- normal but inadequate owing to excessive metabolic n eeds. The causes of high-output heart failure include severe anemia, fever, hyperthyroi dism and pregnancy, etc.劳力性呼吸困描(exeriional dvspnea):随病人体力活动而发生的呼吸困难，休息后可减轻或消失端坐呼吸(orthopnea患者平卧可加重呼吸困难而被迫采取端坐或半卧体位以减轻呼吸困难程度状态夜间阵发性呼吸困难(paroxysmal nocturnal dyspnea):心衰患者夜间入睡后因突感气闷被惊醒，在端坐咳嗽后缓解，入睡后自然滑向卧位,患者呼吸困难又发生，如此反复发作，称夜间阵发性呼吸困难心功能不全(Cardiac insufficiency):从心脏泵血功能下降的完全代偿直至失代偿的全过程充血性心力衰竭(CoimestWe heart Failure):心力衰竭呈慢性经过时，由于钠水潴留和血容量增加，发生静脉淤血噬织水肿及心腔扩大临床综合征.呼吸衰竭(respirator failure.RF):外呼吸功能严重障碍.导致PaO2降低伴/不伴PaCO2增髙病理过程. 限制性通气不足(restrictive hvi)o\ entil玳ion):指吸气时肺泡扩张受限制所引起的肺泡通气不足.常见原因有呼吸肌活动障碍側娜和肺的顺应性降低\胸腔积液或积气等.阻塞性通气不足(obstructive hypoventilation):指由气道狭窄或阻塞所致的通气障碍"常见原因有气道炎症\痉挛\水肿和肿瘤等•若阻塞在胸外,表现为吸气性呼吸困难(inspiratory dyspnea),若阻塞位于中央气道的胸内部分，表现为呼气性呼吸困难(expiratory dypnea)CO2麻醉:当CO2潴留使PaCO2超过10.7kpa(80mmHg)时，可使患者出现头痛，头晕，烦躁不安,言语不淸,扑翼样震颤，精神错乱，嗜睡昏迷，呼吸抑制等.PaCO2为物理溶解于血液的氧所产生的张力.功能性分流(Fimctiomd shun"部分肺泡因病变而通气减少.而流经这部分肺泡的静脉血未经充分动脉化而掺入动脉血，类似动一静脉短路，故称功能性分流，又称静脉血掺杂，此时VA/Q值低于正常.死腔样通气(dead・s”ce like ventilation):部分肺泡血流因血管病变成栓塞而减少，患部肺泡血流少而通气多，这部分肺泡通气不能被充分利用，称为死腔样通气，此时VA/Q值髙于正常.真正分流(true shunt):部分肺泡完全失去通气功能但仍有血流，流经此处的血液完全未经气体交换而掺入动脉血类似解剖性分流，称为真正分流.急性呼吸窘迫综合征(ARDS):是由急性肺损伤(ALI)引起的急性呼吸衰竭,ALI引起呼吸衰竭的机制是由于急性肺泡一毛细血管膜损伤及炎症介质作用，使肺泡上皮和毛细血管内皮通透性增髙，引起渗透性肺水肿，致肺弥散性功能障碍.慢性阻塞性肺部疾病(COPD):由慢性支气管炎和肺水肿引起的慢性气道阻塞.是引起慢性呼吸衰竭的主要原因，机制为:①阻塞性通气障碍②限制性通气障碍③弥散功能障碍④肺泡通气与血流比例失调肺源性心脏病:呼吸衰竭可累计•心脏，主要引起右心肥大与衰竭，即~肺性脑病(pulmonar、encephalopathy):由呼吸衰竭引起的脑功能障碍称为肺性脑病，I型呼衰:低氧血症型呼吸衰竭•根据PaCO2是否升高来判断.肺泡缺氧,CO2潴留致血液H过高,可引起肺小动脉收缩;肺动脉长期收缩，缺氧均可引起无肌性肺微动脉肌化;长期缺氧，血液粘度升高;肺部病变II型呼衰:髙碳酸血症型呼吸衰竭，根据PaCO2是否升高来判断.翹血妞:部分肺泡因病变而通气减少,而流经这部分肺泡的静脉血未经充分动脉化而掺入动脉血内, 这种情况类似动一静脉短路，故称功能性分流，又称静脉血掺杂，此时VA/Q值低于正常.肝功能衰竭(hepatic failure):各种损肝因素使肝细胞发生广泛严重损害，使肝功能发生严重障碍，岀现黄疸\岀血\肾和脑功能障碍等一系列症状的临床综合征.肝性脑病(hemtic enceDhHoDathY):肝性脑病是继发于急\慢性肝功能衰竭和严重悔性实质性肝病的一种神经精神综合征，临床上出现一系列神经精神症状，最终岀现肝性昏迷.氨中毒学说仏性脑病发生是由于肝功能严重受损，尿素合成发生障碍而导致血氨水平增髙，增髙的血氨通过通过血脑屏障进入组织，引起肝功能障碍假性神经递质(false neurotransmitter):在肝功能严重障碍时•体内形成的芳香族氨基酸产物苯乙烯醇胺和羟苯乙醇胺在化学结构与貞•性神经递质去甲肾上腺素和多巴胺极为相似，但生理效能远较真性神经递质为弱,故称它们为假性神经递质.肠源性内毒素血症:许多非格兰阴性菌感染的重症病人及处于应激状态的患者.绝大部分岀现内毒素血症，血浆中内毒素血症主要来源于肠道内毒素的吸收.肝肾综合征(hepatorenal syndrome):指肝硬变失代偿期或急性重症肝炎时傩发于肝功能衰竭基础上的功能性肾功能衰竭.又称肝性功能性肾衰竭.急性肾功能衰竭(acute remd角iliire.ARF):各种原因短期内引起肾脏泌尿功能急剧障碍，抑制机体内环境出现严重紊乱的病理过程，临床表现有水中毒，氮质血症，高钾血症，代谢性酸中毒原尿回漏(ori血讪urine reflux):原尿可经受损肾小管壁处反漏入周国肾间质.除直接造成尿疑减少外. 还引起肾间质水肿，压迫肾小管，造成囊内压升髙，使GFR减少，出现少尿矫枉失衡学说(trade-off hypothesis)是指矫正过度导致新的失平衡,具体讲是由于机体对GRF降低进行代偿时,因代偿引起机体内环境新的紊乱(包括内分泌功能紊乱)，产生新的病理过程.尿毒症(11“1】曲):急\慢性肾功能衰竭发展到最严重的阶段.内源性毒性物质在体内潴留.引起一系列自体中毒症状氮质血症Zzotemi"正常人血淸尿素氮10~15mg%血中尿素\肌酹\尿酸等非蛋白含氮物质的含量增髙. 慢性肾功能不全(chronic renal insufficiency, CRI):各种慢性肾脏疾病进行地破坏肾单位.以致残存的有功能的肾单位不能充分排出代谢产物和维持内环境的恒左，因而体内逐渐出现代谢废物的潴留和水\ 电解质与酸碱平衡紊乱以及肾内分泌功能障碍，称之为慢性肾功能不全.乳酸中樹lactic acidosis)各种原因使机体严重缺氧时，匍萄糖经无氧酵解途径生成乳酸，乳酸过多超出肝脏的利用能力或严重肝脏疾患造成乳酸利用障碍导致血液中乳酸浓度严重升高，引起代谢性酸中毒酮症酸中毒(keto-acidosis)机体匍萄糖缺乏或代谢障碍.脂肪分解加速.大量脂肪酸进入肝脏而形成过多酮体,通体酸性较强，当其量超过外周组织的氧化能力及肾脏排除能力时，血中酮体变会蓄枳病理生理学主要研究方法:animal experiment,clinical observation,epidemeology research Health indicates…physically.socially.mcntally.Among different causes of disease…biolo gical factonphysical factor,chemical factonnutritional imbalance factor.The major intrinsi c causes are-一genetic factor,congenitals factorjmmunologicals factor,psychologicaland so cial factors.A predisposing factor refers to■一promotion or development.Brain death is a state一-response to stimali,brain stem reflexes.and spontaneous respirations 疾病发生的•般规律:process of damage and anti-daniage,altermation of cause and effect,correlation b etween systemic and local regulations 基本机制meural mechanismJiumoral mechanism.cell ular mechanism and molecular mechanismThe ECF volume is lowered in a decreased osmolality in ECF.Hypervolemic h、pona tremia can cause…incieased.dilutcd.swelliiz Severe hvoervolemic hvDonatremia in…de hydration fever.Occurs with identical…isltonic dehydration.The etiology of hypokalemi g—abnormality of transcellular distribution,inadquate intake,excessive losses.In hvpokale mia the effects on…increased,dweased,increascd・The ECG change in hypokalemia…flat,prominent,suppressivexctopic beats.wide.The ECG change in hyperkalemia■一peaked,p rolonges arrhythmiasTo keep a relatively ncidity.bjsicity.Ackb base imbalance―water-electrolyte.The acids formed 一-volatile acids,nonvolatile acids.A normal range—Dete conipensation.acidosis.alkalosis.High AG metabolic一-lactic acidosis,diabetic betoalidosis,renal failure. The buffer systems-一PHJimps.kidneys.The main alterations—cardiac arrhythmiasjiegati ve inotropic nction.acidosis induced bv Chronic metabolic.In chronic “SDiratorv-一kid neys.The disturbance—pulmonaiyA high concentration…hypertension.edema.Changes o FPaCO2…acidosis.alkalosis.Calculation of AG…metabolic acidosisjnixedEtiology of hypotonic…decrease PO2 of inspired air,extermal respiratory disfunction,ven ous-to-arterrial shunts.When hypoxia,the—-hi^h-altitude pulmonary,central respiratory.Dvsf unction of the-一edema.The low一-metabolic states.The positive central…PGE,Na/Ca iatio.cAWIRCRH.NO.The development of…the ferves cense stage,the persistent febrile stageJhe defervescense stageThe principal neuroendocrine…LC/NE.HPA.Stressors can be—extenud environmental stressorsjnternal stressor.psycho-social stressorsThe anticoagulant svstem-—inhibition.AT」ILthiombomodiilin・Drotcin system.The active component■一TEfactor Vila.extrinsic.The mechanisms of-一extensive-tissue injuries,damage of vascular endo什lelial cells,destuction of blood cells,activation of Dlatelet.In DIC cans ed-一Endotoxin,TF,FDPs・The mechansims of■一consumption of coagulation factors,second ary fibrinolysis,formation of FDPs.On the diagnosis-一3P test.D-dimer test.The clinical manifestations■一bleeding,organ dysfunctioirshock.MAHAThe factors that■一duration of ischemia,collateral circulation,dependency on oxygen supp ly,condition of rcDerfusion.The Dathogenesis of—free radicals,calcium overload.neutrophil sactivation.The three biological-—xanthine oxidase pathwayjieutrophils pathwayjnitocho ndria pathwayCauses of high・oiitDiit―severe cmemia.hvDerthvroidism.fever.D22nancv.The cardiac com pensation一・increasing outputjncreased heart rate and cardiac contractility,myocaedial hyp eitroDhv.IVIvocardial hvDertroDhv can・—concentric hypercrophy.eccentric hypertrophy.Hea rt Failure may-一diactolic dysfunction,systolic dysfunctionjnyocardial excessus hypertroph y,altered signal transduction.Cardiac output can一-svstolic,diastolic.Cardiac output depe nds…heart rate.contmctilitvQieload.jfterloacLThe dysfunction of…reduced influx of extra cellular Ca,altered of SR handling calcium.dysfunction of Ca bingding to troponin ResDirator、failure is—extemal resDieatorv.According to Dathogenesis…ventilation PF,e xchanging RF.If the central—inspiratory,expiiatory,expinitory・The force expiration■一upsi de movement.The blood gas—decreased,increased,dccreased.noi・malortorv Failure could■一respiratoryacidosisjnetablic acidosis,respiratory alkalosis.The main mechanisms—ventilation disordendiffusion impairment,ventilation or peifusion imbalance, theincrease of anatomic shuntThe Factors contribute…an increase in capillary pressure,obstruction of venous and ly mph flow through the liverjecrease in colloidal osmotic pressure,solt and water retentio n.Iiicrease in AAA…noimal neurotransmitters,false neurotnmsmitters.The most importa nt precipitating■一nitrogenous overload .The effects of ammonia—impaiirnerH of engergy metabolism in brain,alteration of neurotransmittersjnhibiting action on nerve cells mem braneThe patients with—oliguria or anuria,water intoxicationJiyperkalemia^metabolic acidosis, azotemia.The causes and mechanisms-一renal ischemia,glomenjlar diseases,tubular obtmc tion,original urine reflux,renal cell injury.In the oliguric…hyperkalemia.Three theoretica 1 hvDothesis■一intact nephron hypothesis,trade-off hypothesis,glomerular hyperfiltration hy pothesis.The mechanisms of--EPO production 下降,bone marrow suppressive,dysfunction of utilization of iron and protein,hemolysis and gastrointestinal blood loss.The median isms of-一dimibished absorption of Ca from the gut,overproduction of PTAJisorded VD metabolism,chronic metabolic acidosis细胞凋亡相关酶:核酸内切酶‘caspase家族.DNA片段化是细胞凋亡主要特征内生致热原种类：IL-1 JNF.IFN.IL-6, 应激性溃疡发生机制:黏膜缺血.糖皮质激素作用.其他因素:酸中毒等肝性脑病发病机制:ammoni J intoxication hypothesis,false neurotransmitter hypothesis,GAB A hypothesis,amino acid imbalance hypothesis:支链aa(BCAA)升高，芳香族aa(AAA)减少慢性肾衰机制:intact nephron hypothesis,glomerular huperfiltration hypothesis山ade・off hypo thesisjubular and interstitial cells lesion hypothesis 常见独立风险因子:RAS激活，氧化应激,蛋白尿，醛固酮。
