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1、精品_精品资料_病理生理学重点总结（ Pathophysiology highlights）急性肾功能衰竭（急性肾衰竭）在各种致病因素下,引起肾泌尿功能急剧下降, 导致排泄功能及调剂功能障碍, 以致代谢产物潴留, 水、电、酸碱平稳紊乱.一、缘由与分类1、肾前性急性肾衰（功能性肾衰）肾衰竭或肾功能衰竭缘由：低血容量（大出血、创伤、脱水等）心输出量降低（心衰）肾血液灌流量急剧？血管床容积扩大（过敏性休克）2、肾性急性肾衰（器质性肾衰）肾衰竭或肾实质性肾衰缘由：肾实质病变（1） ）急性肾小管坏死：约占 2/3肾缺血肾中毒：重金属,药物和毒物. 生物毒素（蛇毒）.内源性肾毒物（ HB、肌红蛋白）（2）
2、 ）肾脏本身疾病可编辑资料 - - - 欢迎下载精品_精品资料_肾小球性疾病：（肾小球肾炎、狼疮性肾炎） 间质性肾炎血管性疾病：恶性高血压,双侧肾动脉血栓形成或栓塞等. 3、肾后性急性肾衰（堵塞性肾衰）肾衰竭或梗阻性肾功能衰竭缘由：双侧尿路结石盆腔肿瘤尿路梗阻前列腺肥大药物结晶等 二、发病机制1.肾血流量？（1） ）肾灌注压？（2） ）肾血管收缩：交感 - 肾上腺髓质系统兴奋. RAA激活.前列腺素产生？（3） ）肾缺血 - 再灌注损耗肾血管内皮细胞受损、肾小管坏死 2.肾小管损害3.肾小球超滤系数？（反映肾小球的通透才能,取决于滤过面积和滤过膜通透性.）可编辑资料 - - - 欢迎下载精品_
3、精品资料_三、少尿型急性肾衰分期及机能代谢变化1.少尿期（1） ）尿的变化：尿量：少尿（ 400ml/ 天）或无尿（ 100ml天）尿成分：肾小管损害有关（2） ）水中毒少尿分解代谢加强,内生水水潴留稀释性低钠血症细胞水肿输液过多（3） ）代谢性酸中毒酸性产物排出可编辑资料 - - - 欢迎下载精品_精品资料_肾小管泌 H +、NH4+, HCO3-酸 20 / 1 代谢性酸中毒分解代谢加强,固定酸生成（4） ）高钾血症（最严峻并发症）缘由：尿钾排出组织破坏,细胞内钾释放重吸取 碳酸氢钠 / 碳可编辑资料 - - - 欢迎下载精品_精品资料_代酸致细胞内钾外移输入库存血、摄入高钾食物（5） ）
4、氮质血症（ NPN 40 毫克/ 分升）蛋白质代谢产物排出GFR| 血中非蛋白氮（ NPN）（尿素、肌酐、尿酸等）组织破坏蛋白质分解代谢 -2.多尿期（1） ）多尿形成机制？肾血流量和肾小球滤过功能渐复原.？新生的小管上皮细胞浓缩功能低下.？血中尿素等大量滤出,渗透性利尿.？肾间质水肿消退,堵塞解除.（2） ）多尿期功能代谢变化尿量增多,大于 400 毫升/ 天.可编辑资料 - - - 欢迎下载精品_精品资料_早期：高钾血症、氮质血症、代酸仍存在.后期：易致脱水、低钾、低钠.易感染.3.复原期慢性肾功能衰竭（慢性肾衰竭） 肾性高血压机制： A. 水钠潴留B. 肾素血管紧急素醛固酮系统激活C.
5、肾脏降压物质生成削减肾性骨养分不良（肾性骨病）或肾性骨病机制： 1、高磷低钙血症与继发性甲旁亢2, vitamin D3 activation barrier: intestinal calciumabsorptiondecreases,the decreaseinbone calciumdeposition 3, acidosis: bone calcium dissolution* Hepatic Encephalopathy: hepatic encephalopathy secondary to acute liver failure or severe chronic liver d
6、iseasesubstantive neuropsychiatric syndrome. The theory of ammonia poisoning.可编辑资料 - - - 欢迎下载精品_精品资料_NH3generatesor clearsblood NH3, interfereswithbrainenergy metabolism, neurotransmitter metabolism, nerve cell membraneaction, and CNS dysfunction hepatic encephalopathy The blood of hepatic encephalo
7、pathy caused by NH3.1. interfere with the energy metabolism of the brainConsume a- keto glutaric acid and interfere with the three carboxylic acid cycle;Consumption of NADHreduced respiratorychain formationby ATP; The synthesisof glutamineconsumption decrease,ATPincrease;The pyruvate dehydrogenase a
8、nd a- keto acid dehydrogenase system were inhibited, affecting the three carboxylic acid cycle.2. , the neurotransmitter changes in the brainHow excitatory neurotransmitters glutamate and acetylcholine.How the inhibitoryneurotransmitter g- amino butyric acid.3. inhibitory effect on nerve cell membra
9、ne The blood BCAA. AAA, the mechanism. Insulin可编辑资料 - - - 欢迎下载精品_精品资料_BCAA muscle tissue uptake and breakdown AAA hepatic uptake and breakdownImpaired liver function, reduce insulin inactivated, so theblood BCAA., AAA. AAA competes with the same vector into the brain.False neurotransmitter Benzene e
10、thanol amine- on - octopamineThe mechanism of hepatic encephalopathy caused by upper gastrointestinal bleeding is that the blood protein and bacteria in the intestine decompose and increase ammonia production, resulting in elevated blood ammonia levelsRespiratory failure respiratory, failure: a seve
11、re respiratory disorder characterized by decreased PaO2 oraccompanied by elevated PaCO2. Respiratory failure can bedividedintohypoxemia hypoxemic,respiratory,failure,type I and hypoxemia accompanied by hypoxemia hypercapnic, respiratory, failure, PaCO2 according to whether or notelevated.The pathoge
12、nesis of respiratory failure1. ventilatory dysfunction可编辑资料 - - - 欢迎下载精品_精品资料_A restrictive ventilatory disorder caused by all factors of alveolar expansion is limited to.The obstructiveventilatorydisorder:dividedintocentraland peripheral airway obstruction of airway obstructionexpiratory dyspnea2.
13、dysfunction of ventilation The diffusion barriersThe alveolar ventilation perfusion imbalance normal value 0.8The function of the VA/Q shunt down The dead space like ventilation VA/Q up The anatomic shuntPathogenesis of pulmonary heart diseasePathogenesis of ARDSThe principle of treatment of respira
14、tory failureI. removing the cause of diseaseTwo. Improve pulmonary ventilation: keep the airway clear可编辑资料 - - - 欢迎下载精品_精品资料_Three. Oxygen inhalation:Type I respiratory failure:high concentrationoxygen suction 50%Type II respiratory failure: a continuous low concentration 30% of low flow oxygenFour.
15、Correctacid-basedisturbanceand protectorgan functionThe pre load - load capacity:in the heartdiastolicencounter load to heart cavityend diastolicvolume end-diastolicvolume, EDV as the index.After the load pressure load encountered: systolic load is encountered when heart ejection resistance.Failure
16、output heart High: cardiac output is higher than the normal level, but lower than the patients heart failure before the level. Common in hyperthyroidism, severe anemia,arteriovenous fistula and so on.In the excitation contraction coupling disorder1. sarcoplasmic reticulum Ca2+ treatment dysfunction(
17、1) the abilityof sarcoplasmicreticulumCa2+uptake decreased ATP deficiency, sarcoplasmic reticulum calcium pump functionto reduce the sarcoplasmic reticulum uptake of Ca2+ decreases, can not fully diastolic myocardial可编辑资料 - - - 欢迎下载精品_精品资料_(2) sarcoplasmic reticulum Ca2+ storage decreasedThe release
18、 of Ca2+ decrease in sarcoplasmic reticulum uptake of Ca2+ and Na+-Ca2+ exchange: relax, sarcoplasmic reticulum Ca2+, myocardial contraction: storageDiminished myocardial contractility(3) the releaseof Ca2+in sarcoplasmicreticulumwas decreasedAcidosis - Ca2+ and sarcoplasmic reticulum binding firmly
19、. Sarcoplasmic reticulum release Ca2+ decrease2. Ca2+ internal flow disorder Intracellular Ca2+ influx:1. voltage dependent Ca2+ channelMembrane depolarization Ca2+ channel opening2. receptor controlled Ca2+ channelNE-b receptor cAMP, Ca2+ channel open3. Na+- Ca2+ switching bodyHeart failure, acidos
20、is, intracellular NE, B receptor and its affinity to Ca2+ channel blocked down可编辑资料 - - - 欢迎下载精品_精品资料_3. troponin Ca2+ binding disorderHeart failure, acidosis, H +, competes with Ca2+, combines troponin, troponin, and Ca2+ binding disordersHeart compensation during heart failure 1, heart rate increa
21、sedSignificance：A certaindegree of heartrateisincreasedand cardiacoutput is increased.Disadvantageous:Increase myocardial oxygen consumption.The hearthas a shortdiastolicperiodand myocardialischemia. As an indicator of the severity of cardiac insufficiency2, myocardial contractility increasedThe mos
22、t common,effective,and importantform of compensation. This positive inotropic effectThis source of tension expansion* myocardial hypertrophy可编辑资料 - - - 欢迎下载精品_精品资料_(1) positive inotropic effect - isometric self regulation increase in pressure loadDoes not change the initial length of myocardial fibe
23、r;The intrinsiccontractionof the myocardium itself increases. Mechanism: positive inotropic action of catecholamines.(2) myocardial tension dilated variable lengthSelf regulation volume, load, increaseDilatation of the heart cavity, accompanied by an increase in volume, accompanied by an increase in
24、 myocardial contractility.Mechanism: Frank-Starlings law Significance: preload. EDV. HereThe initial length of myocardial fiber. HereThe number of coarse and fine filament reactions increased可编辑资料 - - - 欢迎下载精品_精品资料_HereIncreased myocardial contractility Disadvantages: 1 EDV. 2 EDV. Down hereEDP vent
25、ricular wall tension. Down hereWhat is the venous pressure. Myocardial oxygen consumption. HereVenous congestion, edema3. myocardial hypertrophyThe myocardial cell volume was increased by increasing the number of mitochondria, namely, diameter, length increases, the heart weight increased.Type:Eccen
26、tric hypertrophy eccentric, hypertrophy Concentric hypertrophy concentric, hypertrophy Compensatory significance:可编辑资料 - - - 欢迎下载精品_精品资料_Adverse aspects:1. oxygen and nutrients are difficult to diffuse2. lack of biological oxidation process of myocardial cells* myocardial remodeling myocardial remod
27、eling Refers to the adaptive and proliferative changes in thecellularstructure,function,quantity,and geneticphenotype of the heart and the interstitium in response to an increasein heart load during heart failure.The cause of ischemia-reperfusion injury:1. restoreblood supplyaftersystemic circulator
28、ydisturbance2. blood flow recovery after organ ischemia3. after recanalization of a blood vessel Conditions of ischemia-reperfusion injury1. ischemia time2. collateral circulation3. oxygen demand4. reperfusion condition可编辑资料 - - - 欢迎下载精品_精品资料_* freeradicals: refersto the outer railhas a generalsingl
29、e unpaired electrons of atoms, atoms or molecules.Reactive oxygen species reactive oxygen * species, ROS: oxygen containing compounds than oxygen in active chemical performance.The mechanism of ischemia-reperfusion injury:Damaging effects of free radicals1. lead to lipid peroxidation2. protein denat
30、uration and enzyme activity decrease 3.DNA breakage and chromosome aberration4. induce proinflammatorycytokinesand inflammatorymediators by oxidative stressMechanism of injury caused by calcium overload1. mitochondrial dysfunction2. activation of calcium dependent degrading enzymes3. promote free ra
31、dical formation4. ischemia reperfusion arrhythmias可编辑资料 - - - 欢迎下载精品_精品资料_5. , excessive contraction of myofibrils Microvascular damage and the role of leukocytes1. ischemia reperfusion leads to inflammatory reaction2. excessiveinflammatoryresponse leads to tissuecelldamage, apoptosis, and necrosis.
32、* myocardialstunningmyocardialstunning:refersto a short time after myocardial ischemia without necrosis,However, changes in structure, metabolism, and function may take several hours, days or weeks after the reperfusion to return to normal.* shock shock: in a variety of reasons hemorrhage, trauma, b
33、urns, infections, allergies under the action of the bodycaused by effectivecirculatingblood volume decreased rapidly,tissue blood perfusion caused a serious shortage of importantorgans seriouspathologicalfunctionand metabolicdisorders.Staging and characteristics of shockI early stage of shock;This s
34、tage is mainly characterized by microcirculatory ischemia, which is also called microcirculatory spasm or ischemic hypoxia Ischemic, anoxia, phase.1. the characteristics of microcirculatory blood perfusion可编辑资料 - - - 欢迎下载精品_精品资料_Less irrigation, less flow, less irrigation two shock stage;This period
35、 with microcirculatory stasis, also known as the microcirculatory stasis period or stagnant anoxia phase Stagnant anoxia phase.1. the characteristics of microcirculatory blood perfusion More irrigation, less flow, more irrigation than flow three late shockThis periodof micro vascularsmooth muscle pa
36、ralysis,lossof reaction to any vasoactive drugs, also known asmicrocirculationfailure;clinicalon the patientat thisstage is often a lack of effective treatment, so called refractoryshock refractory stage.1. the characteristics of microcirculatory blood perfusion No irrigation, no flowCompensatory si
37、gnificance in early stage of shock Maintain arterial blood pressure1) increase the amount of cardiac effort可编辑资料 - - - 欢迎下载精品_精品资料_2) the heart rate increases, the heart contractility strengthens, and the cardiac output is maintained3) peripheral resistance increased Redistribution of systemic blood
38、 flow The relationship between DIC and shock Microcirculation failure shock1, micro thrombosisand embolism - blocked blood flow- reducedblood volume2, extensivebleeding,effectivecirculation,decreased blood volume3, vasoactivesubstances - - vasculardilatation,permeability- - plasma extravasation4, hy
39、poxia, acidosis, myocardial damage, cardiac output: DIC shockChanges of blood rheologyDamage of vascular endothelial cells Shock, ischemia, anoxia, acidosis Here可编辑资料 - - - 欢迎下载精品_精品资料_Impaired vascular endothelial cells HereTissue factor releaseThe decrease in activation Coagulation systemHereDIC f
40、ormationTissue factor release, TF Imbalance of TXA2-PGI2Shock, DIC, exacerbation of shockBy the systemic inflammatory response syndrome systemic inflammatory response syndrome, SIRS: nature is the body out of control, self sustained amplification and destroy its disseminated inflammation, inflammato
41、ry cell activation, inflammatory mediators overflow into plasma, and thus causes inflammation of distant place.* multiplesystem organ failuremultiplesystem organ failure,MSOF: severe trauma, infection, shock or recovery after the failure of two or two or more organ systems, happen in a short可编辑资料 -
42、- - 欢迎下载精品_精品资料_period of time. Predisposing factors of DIC1, the mononuclear phagocyte system is impaired 2, hepatic dysfunction3. Hypercoagulability4. Microcirculatory disturbance* two D- dimer examination: two D- dimer D-dimer:DD is a fibrinolytic enzyme decomposition of fibrin Fbn product.D- two
43、 is an important indicator of secondary fibrinolysis. Pathogenesis of DIC:1. injury and activation of vascular endothelial cells 2., tissue damage, tissue factor into the blood3. damaged blood cells4. , exogenous procoagulant substances such as heterologous particles into the bloodDIC bleeding mecha
44、nism:1 coagulation substances are reduced by a large amount of可编辑资料 - - - 欢迎下载精品_精品资料_consumption2. Secondary and / or primaryactivationof fibrinolyticsystem 3, FDP form* stress:the body stresson neuroendocrineresponses mainlynonspecific defense reactions appear various factors when stimulated.The d
45、efensive significance of locus coeruleus sympathetic nerve adrenal medullary response1 、 heart rate, cardiac contractility, cardiac output.BP. The blood supply of the organization. 2, glycogen and fat decomposition.Conducive to the increase in energy demand.3, the blood redistribution, to ensure the heart, brain, bone Skeletal muscle blood supply.4 bronchiectasis provides more oxygen.5, it can promote the secretion of many hormones: Such