病生名解大题整理

病理名解大题1.Fundamental pathological processes基本病理过程Is defined as some common and whole set functional, metabolic and structural alterations in different disorders2. Health健康State of complete physical, mental, and social well-being and not merely the absence of disease and infirmity3.Desease 疾病Aberrant manifestation of deregulated homeostasis caused by harmful agents4. Hypertonic dehydration (Hypovolemic hypernatremia)高渗性脱水The dehydration in which the water loss is in excess of salt loss and the ECF of the body is hypertonic is termed of hypertonic dehydration.5. Hypotonic dehydration (Hypovolemic hyponatremia)低渗性脱水的The dehydration in which the salt loss is in excess of water loss and the ECF of the body is hypotonic is termed of hypotonic dehydration.6. Hypokalemia低钠血症Serum [K ] 3 5 l/L Serum [K+]<3.5mmol/L, mayor may not be associated with K deficit.7. Hyperkalemia高钠血症Serum [K ] 5 5 l/L di l Serum [K+]> 5.5mmol/L, a medical emergency8. Cell edema细胞水肿当缺氧、中毒及线粒体ATP产生时，膜钠泵功能降低，钠和水进入细胞内，导致细胞内水分过多聚集，细胞肿胀，称为细胞水肿When hypoxia,toxin and mitochondrial ATP is produce ,the function of calcium pump inside the membrane decrease ,sodium and water enter the cell ,which cause the over aggregation of water ,the cell swell ,called cell edema水肿：过多的液体在组织间隙或体腔内聚集称之为水肿An abnormal accumulation of fluid in the cells, tissue spaces, or cavities of the body, also known as dropsy9. hyperdepolarization block超极化阻滞When in acute hypokalemia, [K+]i / [K+]e↑,cause RMP more negative than normal, excitability ↓,the patient appear muscle weakness, flaccid（弛缓性）paralysis, smooth muscle symptoms 10. depolarization block去极化阻滞In Severe hyperkalemia, ratio of [K+]i to [K+]e↓→RMP decreased to level of TMP, the patient appear muscle weakness, paralysis, dizziness, coma symptoms11. Anion gap (AG)阴离子间隙is the difference between plasma unmeasured anions and the unmeasured cations12. Paradoxical alkaluria反常性碱性尿In the Renal tubular acidosis ,H+ excretion is decreased or HCO3- reabsorption is decreased ，causing the urine pH is alkali instead of acidic13. Respiratory acidosis呼吸性酸中毒It is the acid –base disorder characterized by pH decrease caused by primary increase of PaCO2 or H2CO314. Paradoxical aciduria反常性酸性尿In alkalosis, hypokelemia promotes H+ excretion and HCO3- retention, causing the urine pH is acidic instead of alkali15. Hypoxiais the most common pathological process, in which tissue cells can not obtain enough oxygen or can not fully utilize oxygen, thus leading to metabolic, functional, even structural changes 16. Hypotonic hypoxia低张性缺氧Is a kind of hypoxia characterized by a decrease of PaO217. Hemic hypoxia (isotonic hypoxia )血液性缺氧Is a kind of hypoxia characterized by the decrease of HB amount or affinity18.blood capacity 血氧容量Is the maximum amount of O2 that can be potentially combined to hemoglobin in 100ml blood 19.Reperfusion injury 再灌注损伤refers to damage to tissue caused when blood supply returns to the tissue after a period of ischemiaIschemia –reperfusion injury : the restoration of blood flow after transient ischemia may be associated with further reversible cell damage ,which is called ischemia –reperfusion injury20. Calcium overload 钙超载The abnormal increase of intracellular calcium which causes cell injury21. No reflow phenomenon 无复流现象is the failure of blood to reperfuse an ischemic area after the physical obstruction has been removed or bypassed22.Myocardial stunning 心肌抑顿is the reversible reduction of function of heart contraction after reperfusion not accounted for by tissue damage or reduced blood flow23.Calcium paradox钙反常Refers to that the restoration of that calcium concentration in perfusion solution after transient no calcium perfusion may induce lethal cell injury24. Cardiogenic shock心源性休克Is a kind of shock caused by failure of heart pump function ,sharp decrease of heart output , decline of effectively circulatory blood volume25. MODS （Multiple organ dysfunction syndrome）多器官衰竭证是指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定必须靠临床干预才能维持的综合症When in severe trauma and shock ,it is the presence of altered organ function in acutely ill patients such that homeostasis cannot be maintained without intervention. It usually involves two or more organ systems26.CARS(compensatory anti-inflammatory response syndrome )代偿性抗炎反应综合征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过于强烈的内源性抗炎反应When infection or trauma ,the organisms produce the intense endogenous anti-inflammatory response which can reduce the immune function and increase susceptibility to some infection 27.Auto blood transfusion自身输血results from constriction of the capacitance vessel promoting venous return28.Auto fluid perfusion自身输液Auto-perfusion results from the decreased capillary hydrostatic pressure promoting tissue fluid circumfluence29. Disseminated/diffused intravascular coagulation(DIC)弥漫性血管内凝血A disorder of widespread micro-vascular thrombosis caused by activation of coagulation cascade with Bleeding, Shock, Organ dysfunction, Hemolytic anemia30. Microangiopathic hemolytic anemia微血管病性溶血性贫血Is a kind of special anemia characteristic characterized by schistocyte in blood smear, morphology of schistocyte are helmets ,triangular and kite-shaped, it is easy broken标准碳酸氢盐SB: blood 〔HCO3-〕at PaCO2 40 mmHg, T=38°C, SaO2=100%;实际碳酸氢盐AB: blood 〔HCO3-〕at actual body conditions;缓冲碱BB: all buffer bases in the blood;碱剩余BE: amount of acid or base used for titration of blood pH to 7.431.Acute Renal Failure急性肾衰A pathological process that the kidneys lose the function abruptly and thus leads to disturbance of internal homeostasis32.trade-off 矫枉失衡机体产生的某种代偿机制在发挥某种溶质平衡的适应性反应的同时，对其他系统产生有害作用，导致机体内环境紊乱The organisms produce some compensatory mechanism harmful to other system when it play the adaptive response of some solute balance, resulting internal environment disturbance Trade-off hypothesis 矫枉失衡假说：indicates that as the nephrons are progressively destroyed ,increased blood concentration of some solutes stimulates over secretions of some regulatory factors in order to increase the excretion function33. stress应激Also called stress response ,is an organism's response to a stressor such as an environmental condition or a social ,psychological factors stimulus.34. Fever发热is defined as a body temperature above the normal range due to an increase in the temperature regulatory set-point35.Hyperthermia高热is elevated body temperature due to failed thermoregulation that occurs when a body produces or absorbs more heat than it dissipates.36.Endogenous pyrogen 内生致热原Are described as the cytokines including fever ,which are produced and release by EP cells ,such as interleukin-1,TNF.37. hepatic encephalopathy肝性脑病Injury of hepatic cells or kupffer cells result in dysfunction of metabolism, synthesis, detoxication and immunity, organisms can appear Jaundice, bleeding, infection, hepatorenal syndrome, hepatic encephalopathy, this is called hepatic encephalopathy38. Hepatic Encephalopathy肝功能不全A complex, potentially reversible disturbance in central nervous system that occurs as a consequence of severe liver diseases39.False Neurotransmitter假性神经递including octopamine羟苯乙醇and phenylethanolamine苯乙醇胺, which have similar structure but much weaker activity than the true neurotransmitters40.Dead space-like ventilation死腔样通气111It indicates that the blood flow in the ventilated alveoli is reduced because of disease ,so the air in these alveoli cannot be exploited sufficiently .this situation is just like dead space ventilation41.Restrictive hypoventilation限制性通气不足It means hypoventilation caused by the restriction of alveolar dilation or inflation during inspiration42.Equal pressure point等压点The airway area where airway pressure is equal to intrathoracic pressure43. Functional shunt功能性分流Because of obstructive or restrictive ventilation dysfunction , the involved alveoli have hypoventilation but their blood flow doesn’t redu ce ,thus the radio of VA/Q is lowed ,leading to the venous blood passing through the alveolar capillaries to flow into pulmonary vein without enough oxygenation .this condition is called functional shunt ,just like artery-vein shunt44. Cardiac insufficiency心功能不全Structural and functional changes of heart→Pump/refill↓→CO↓→Ischemia Venous stasis 45.Heart failure心力衰竭111Heart failure is the inability of the heart to supply adequate blood flow and generate a cardiac output sufficient to meet the metabolic demands of the body46. Brain Death脑死亡Is a state of permanent irreversible cessation of whole brain acitivity .at that time ,the function of the patient’s body as a whole body has stopped forever1.What kinds of dehydration is easy to cause shock ? ①Volume of ECF decrease ② ECF transported to ICF ③ Thirsty is not obvious,so the patient don’t drink actively ④ADH release is inhibited2.Effects of Hypokalemia on acid Effects on acid--base balance ①H-K exc hange across cell membrane↑ ②renal hydrogen ion excretion↑3. Metabolic acidosis (1) CausesExcessive intake of fixed acids, salicylate drug Excessive production of fixed acids, e.g., hypoxia Decreased acid excretion, e.g., renal dysfunction Excessive loss of bicarbonate, e.g., diarrhea (2) Compensation of metabolic acidosis 1) Extracellular buffering --- immediately:2) Respiratory compensation --- rapid : ↑↑Ventilation in 10 min, maximal in 12-24 h 3) Intracellular buffering --- in 2-4 h: H+ —K+ exchange →hyperkalemia4) Renal compensation: Start to work in several hours, maximal in 3-5 d more efficient than respiratory compensation. From utilizing the phosphate buffer shift to ammonia production. (3) influences on Cardiovascular system and machines a) pH<7.2 →Decreasing myocardial contractilityb) pH<7.0 → ↓myocardial responsiveness of β-adrenoceptor to catecholamines → ↓ cardiac outputc) Cardiac arrhythmiaAcidosis → hyperkalemia → arrhythmia↓myocardial responsiveness to catecholamines → arrhythmia d) Vasodilation↓responsibility of α-adrenoreceptor in vasculature → ↓ cardiac output (4) machines of High AG type ①Increased production of organic acids.②Acid intake – salicylate etc.③Retention of sulfates, phosphates etc.4. Ischemic Anoxia Phase (Stage1/compensatory stage ) of shock 缺血缺氧期 (1)PathogenesisBleeding→decrease of effectively circulatory blood volume→Sympathetic -adrenal system activation→Extensive constriction→Hypoperfusion (2) 特征/变化：缺血 ①微循环小血管持续收缩micro small vessel continuous contraction ②毛细血管前阻力↑↑>后阻力↑he Precapillary resistance is more than postcapillary resistance ③关闭的毛细血管增多the number of closed capillaries increase ④血液经动–静脉短路和直捷通路迅速流 入微静脉The blood flow through the artery-veinshunt and rapidly flow into the vein thoroughfare channel⑤灌流特点：少灌少流、灌少于流The perfusion characteristics: less irrigation less flow, irrigation is greater than the current(3) Compensatory Mechanisms①Autotransfusion results from constriction of the capacitance vessel promoting venous return②Autoperfusion results from the decreased capillary hydrostatic pressure promoting tissue fluid circumfluence③Redistribution of Blood Flow is the third-line defensive response which ensure adequate blood flow through the brain and heart.(4) Compensatory influences on body①benefit to sustain the arterial BP②benefit to supply blood to heart and brain(5)Clinical Manifestations↓Pulse Pressure decrease , ↓Diastolic Pressure decrease ,↑Systolic Pressure increase , ↑ HR↓ Urine output ,Cold and moist skin5. stagnant hypoxia phase(stage 2/decompensatory stage 淤血缺氧期(1)特征：淤血前阻力血管扩张，微静脉持续收缩The precapillary resistance vessel dilation, micro vein continuous contraction前阻力小于后阻力The Precapillary resistance is less than postcapillary resistance毛细血管开放数目增the number of open capillaries increase灌流特点: 灌多流少，灌大于流The perfusion characteristics: multi irrigation less flow, irrigation is greater than the current(2) Mechanisms①Acidosis②Sympexis,Leucocyte conglutination,Platelet adhesion→postcapillary resistance↑③increaseing of Histamine and Adenosine NO→vasodilation ,permeability ↑→precapillary resistance↓All of those cause congestion ，Venous return↓↓，Bp↓↓6. 简述MODS的发病机制①全身炎症反应失控systemic inflammatory response is out of control②促炎-抗炎介质平衡紊乱The pro-inflammatory and anti-inflammatory mediators balance disorders③气管微循环灌注障碍The tracheal microcirculation perfusion④高代谢状态The high metabolic state⑤缺血再灌注损伤The ischemia reperfusion injury(1) Pathogenesis①Alteration in renal hemodynamicsRenal perfusion ArrayRenal vasoconstrictionGFR↓Renal ischemic-reperfusion injuryRenal hemorheology abnormality②Glomeruli injury③Tubular lesions1) Tubuloglomerular feedback2) Tubular backleak of ultrafiltrate3) Obstruction(2)Oliguria type of ARF(包括ATN急性肾小管坏死少尿)A. Oliguria phase:Disorders of internal homeostasis(1) AzotemiaBUN, creatinine, uric acid nitrogen↓(2) Metabolic acidosis▪Catabolism↑→acidic products↑▪Acid excretion↓▪Secretion of ammonia and hydrogen↓▪Resorption of HCO3-↓(3) Water retention↑Catabolism→→endogenous water↑→→Diluted hypoNa, Edema/water intoxication(4) HyperkalemiaK+ Excretion↓Transfer of K+ from intracellular to extracellular↑（catabolism↑, acidosis）Distal tubular K+-Na+ exchange ↓（hypoNa）B. Diuresis phaseMechanisms of diuresis:(1)Non-integrated function of new grow tubules(2)Accumulation of urea during oliguria phase (leads to osmotic diuresis)(3)Relieve of the tubular obstruction9. Chronic Renal Failure(1) PathogenesisA) . Intact nephron hypothesisAdaptation mechanism:Nephron destroyed, the remaining counterparts adapts by increasing GFR, tubular reabsorptionand excretionWhen the intact nephron is decreasing to a certain degree, it goes to non-compensatory stage→CRFB) Glomerular hyperfiltration hypothesisdestroy nephron→GFR→albumin in filtrateC) Trade-off hypothesisHyperphosphatemia→hypocalcemia→PTH→renal phosphate excretory function→plasma [Pi] level back to normal (corrected an abnormality)PTH↑→osteosclerosis caused by remodeling and redistribution of bone and osteolysis (caused new lesions)D) Tubular and interstitial injuryIt can result from glomerular (chronic glomerulonephritis), interstitial (chronic pyelonephritis), tubular or vascular (arteriolar nephrosclerosis) damages(2) Urine:▪ from diuresis, nocturia to oliguriabecause nephron is destroyed , GFR is decreaseed▪ diuresisflow rate of initial urine is rapid ; osmotic diuresis; function of urine concentration is reduced(3) AcidosisEarly stage of CRF : Secretion of H+ and resorption of HCO3-↓Compensatory resorption Cl- from intestinal↑(4) Hypocalcemia in chronic renal failure①Hyperphosphatemia: [Ca]•[P] = coefficient, [P] , [Ca]②Disorder in VitD activation: 1 hydroxylase synthesis③Decreased absorption from intestinal: disturbance in gastrointestinal function caused by renal toxin, and decrease in activated 1,25 (OH)2-ViD310. Hepatic Encephalopathy(1)Four hypotheses : Ammonia intoxication, False neurotransmitters, amino acid imbalance, GABA hypothesis(2) Ammonia intoxication★Causes of Blood Ammonia Elevation-▪ Overproduction①Intestinal mucosa congestion, edema, bacterial activity increased②Digestion function reduced, lots of protein stay in the intestinal tract③Hepatorenal dysfunction, decreased urine excretion④Kidney produces ammonia⑤Muscle produces ammonia▪ Clearance impairments①Disrupted urea cycle,ATP deficiency, Enzyme inactivation, Substrate deficiency②Portal-systemic shu nt, intestinal ammonia doesn’t go to the ornithine cycle★Influences on brain①Disrupting energy production②Disrupting neurotransmission③Disrupting membraneDead-space like ventilation13. 为什么单纯弥散功能障碍不伴PaCO2升高(CO2是脂溶性的，其弥散速度较O2快，易达到平衡：故单纯弥散障碍主要表现为PaO2下降，而不伴有PaCO2升高14. excitation-contraction coupling dysfunction in the heart failure⑴Calcium influx dysfunction▪ Receptor operated calcium channel dysfunction①Endogenous NE↓②β1-AR↓，Sensitivity to NE↓③Gs↓、Gi/Gs↑④AC activity↓•Reduced calcium channel protein levelL-type channel protein↓，mRNA↓⑵Calcium handling by SR dysfunction▪ Re-uptake: ATP-dependent pump activity decrease▪ Storing decrease▪ Release : SR Ca2+ content decreasemRNA and protein level are both found to reduce in heart failureHydrogen increases affinity of calcium and its binding protein, so the calcium is difficult to be released.⑶Troponin binding dysfunction：H+ compete with Ca2+ binding to troponinReduced sensitivity of immature TnC to Ca2+15. Mechanisms for heart failure①Weaken of cardiac contractility(1) Damage of contraction-related proteins(2) Myocardial metabolic dysfunction(3) Dysfunction of EC coupling②Abnormity of diastolic properties of ventricle(1) Delayed calcium decrease(2) Impaired dissociation of the actin-myosin complex(3) Decreased diastolic potential energy of ventricles(4) Reduced compliance of myocardium③Asynergia of ventricular contraction and relaxation⑴Reduces the forward flow of blood through the heart⑵Abnormal interventricular septal wall motion⑶Reduced diastolic filling time⑷Prolonged mitral regurgitation duration16. [H+]↑→myocardium contractility↓17. Myocardial hypertrophyoverload of myocardium: Preload↑Afterload↑Mechanism of decompensation1）Reduced energy supply2）Energy utility dysfunction3）Excitation-contraction coupling dysfunction4）Collagen fiber↑→Compliance↓10 /。