病理生理学名词解释资料及问答题
病理名解和问答
三、名词解释1、病理生理学2、基本病理过程3、疾病概论4、系统病理生理学六、简答题、1、病理生理学的主要内容有那些？七、问答题1、病理生理学的主要任务是什么？2、什么是基本病理过程？请举例。
三、名词解释1、疾病2、不完全康复3、brain death4、诱因5、病因6.遗传性疾病7、先天性疾病8、免疫性疾病9、免疫缺陷病10、自身免疫性疾病六、简答题1、疾病发生发展的一般规律有哪些？2、什么是脑死亡，其判断标准有哪些？3、引起疾病的原因有哪些？4、什么是先天性疾病，它与遗传性疾病有何区别？5、什么是分子病，分子病主要包括哪些？七、问答题1、试举例说明什么是疾病发展的因果转化规律。
2、什么是疾病的原因、条件和诱因？三者关系如何？三、名词解释1、脱水2、高渗性脱水3、低渗性脱水4、等渗性脱水5、water intoxication6、低钠血症7、高钠血症8、低钾血症9、高钾血症10、反常性酸性尿11、反常性碱性尿12、肾小管性酸中毒13、低镁血症14、高镁血症15、抗利尿激素分泌异常综合征六、简答题、1、简述低渗性脱水引起外周循环障碍的机制。
2、简述高渗性脱水早期出现尿少、尿钠浓度增高的机制。
3、简述低钾血症对神经－肌肉的影响及其机制。
4、简述高钾血症对心脏的影响及其机制。
5、简述低镁血症对神经－肌肉的影响及其机制。
6、简述低镁血症对钙、钾的影响及其机制。
七、问答题1、钾代谢紊乱与酸碱平衡紊乱有何关系？2、某患儿腹泻4天，每天水样便10余次，试分析该患儿可发生哪些水电解质紊乱？3、试述创伤性休克引起高钾血症的机制。
三、名词解释1、标准碳酸氢盐（SB）2、实际碳酸氢盐（AB）3、AG4、二氧化碳分压（PaCO2）5、代谢性酸中毒6、PH7、BB 8、BE9、AG增高型代谢性酸中毒10、呼吸性酸中毒11、代谢性碱中毒12、呼吸性碱中毒13、AG正常型代谢性酸中毒14、肾小管性酸中毒六、简答题1、频繁呕吐易引起何种酸碱平衡紊乱？为什么？2、为什么急性呼吸性酸中毒的中枢神经系统功能紊乱比代谢性酸中毒明显？3、简述严重酸中毒易引起休克的机制？4、简述机体有哪些酸碱平衡的调节机制？5、简述代谢性酸中毒对机体的主要影响。
病理生理学重点 名词解释与简答题
病理生理学重点名词解释与简答题（Key terms of pathophysiology Interpretation and brief answer）First, the noun explanationThe basic pathological process: mainly refers to a variety of diseases may occur, common, complete sets of functions, metabolism and structural changes.Health: health means not only sickness or illness, but also a complete, physical, mental, and social state of being.Disease: disease is under certain conditions caused by the cause of damage, due to the body's self regulatory disorder and the occurrence of abnormal life process.Etiology: a cause of disease that is characteristic of the disease and is known as the cause of the disease.Incentives: factors that contribute to the development of disease are called triggers.Brain death (brain death): the permanent cessation of the function of the organism as a whole is a permanent loss of the function of the brain. At present, the standard of brain death above the foramen magnum is generally used.Hypotonic dehydration: also called hyponatremia of low volume, characterized by losing Na+ more than dehydration, serum Na+ concentration <130mmol/L, plasma osmotic pressure <280mmol/L, accompanied by a decrease in extracellular fluid volume.Hypertonic dehydration: also known as low volume hypernatremia, characterized by more water loss than loss of Na+, serum Na+ concentration of >150mmol/L, plasma osmolality, >310mmol/L, extracellular fluid volume and extracellular fluid volume are reduced.Water intoxication: high solubility hyponatremia, characterized by decreased serum sodium, serum Na+ concentration, <130mmol/L, plasma osmotic pressure <280mmol/L, but the total body sodium is normal or increased, the patient has water retention, so that the volume of fluid increases significantly.Dehydration fever: because of the decrease of water from the skin, the heat is affected, leading to elevated body temperature, called dehydration fever.Edema: excessive fluid that is called edema in the interstitial space or inside the body cavity.Hyperkalemia: serum potassium levels are higher than 5.5mmol/LHypokalemia: serum potassium levels below 3.5mmol/L.Disturbance of acid-base balance: the excessive acid base overload, serious deficiency or regulatory disturbance caused by pathological conditions lead to the PH abnormal condition caused by the destruction of acid-base homeostasis in the environment.Metabolic acidosis: a type of acid-base disturbance characterized by an increase in extracellular fluid H+ or a primary decrease in HCO3- and a decrease in PH.Respiratory acidosis: a CO2 disorder or excessive intake causes a disturbance of acid-base balance characterized by a primary increase in plasma [H2CO3] and a decrease in PH.Metabolic acidosis: extracellular liquid increase or loss of H+, [HCO3-] in plasma increased and PH increased primaryacid-base disorders characterized by type.Respiratory alkalosis: a type of acid-base disturbance characterized by hyperventilation of the lungs and primary decrease in plasma [H2CO3] and elevated PH.Mixed acid-base disturbance: there are two or three simple types of acid-base disturbances in the same patient.Hypoxia (hypoxia): pathological changes in cellular metabolism, function, and morphological structure resulting from reduced oxygen supply or impaired oxygen use.Cyanosis (cyanosis): when the uniform concentration of deoxygenated hemoglobin in the blood capillary of more than 5g/dl, the skin and mucous membranes were purple.Type four hypoxia: hypoxia hypoxia, blood type hypoxia, circulatory hypoxia, tissue hypoxia.Enterogenous cyanosis: methemoglobinemia due to eating leadsto a large number of hemoglobin oxidation caused by.Shock: this word by Shock, and English shock, various strong risk factors acting on the body, the circulation decreased dramatically, tissue and organ perfusion of microcirculation is seriously insufficient, and systemic critical pathological process of vital organs function, metabolic disorder serious.MODS (multiple organ dysfunction syndrome): refers to the severe trauma, infection, shock, the original organ dysfunction of patients at the same time or within a short period of time have appeared more than two organ system dysfunction that homoiostasis must rely on clinical intervention to maintain syndrome.Systemic inflammatory response (SIRS): a systemic inflammatory response syndrome that results from uncontrolled, self sustained enlargement and self destruction caused by infection or non infectious agents acting on the body.Compensatory anti-inflammatory response syndrome (CARS): when an infection or trauma occurs, the organism produces an endogenous anti-inflammatory response that is associated with an increased immune response and an increased susceptibility to infection.DIC (disseminated intravascular bleeding): a role in the pathogenic factor, the coagulation system was activated and induced by micro thrombosis, or secondary fibrinolysis, resulting in bleeding, shock, organ dysfunction and microangiopathic hemolytic anemia in a pathological process.FDP fibrin degradation products: plasmin hydrolyze various fragments produced by Fbg and Fbn.Split cell: a special variant of the shape of red blood cells,Called schistocyte, shape, star, moon shaped helmet, referred to as the red cell debris. The fragment is high in brittleness and susceptible to hemolysis.Heart failure: cardiac pump dysfunction caused by various causes, and a negative or relatively reduced cardiac output that fails to meet the metabolic needs of tissue.Myocardial tension (muscle) derived dilatation:The source of expansion: reduce the myocardial tension due to stroke volume, the ventricular end diastolic volume increased, pre load led to the increase of the initial length of the muscle fibers increased, then enhance myocardial contractility, metabolism increases stroke volume, heart cavity enhanced myocardial contractility with this expansion called heart source expansion.Myogenic expansion: long-term volume overload and heart failure caused by dilated cardiomyopathy, mainly caused by excessive sarcomere stretch, the heart cavity enlargement, heart cavity with the excessive stretch and decreased myocardial contractility with expansion called myogenic expansion.Respiratory failure: a pathological process in which the arterial blood oxygen pressure is below normal and accompanied by or without elevated carbon dioxide partial pressure due to severe external respiratory dysfunction.Restrictive hypoventilation: alveolar ventilation caused by restricted expansion of the alveoli during inspiration. Obstructive hypoventilation: a ventilatory disorder caused by narrowing or obstruction of the airways.Functional shunt: part of alveolar ventilation lesions significantly reduced blood flow and weight, not less, even because of inflammatory hyperemia to increase blood flow (such as lobar pneumonia, early) ratio of alveolar minute ventilation and pulmonary blood flow per minute was significantly reduced, so that the flow through this part of alveolar venous blood without sufficient artery can mixed with arterial blood, the similar arteriovenous short circuit, called functional shunt, also known as blood doping.Dead space ventilation: under certain etiological factors, partial alveolar blood flow can be reduced, VA/Q can be significantly increased, less alveolar blood flow and ventilation, alveolar ventilation can not be fully utilized, become dead cavity like ventilation.Pulmonary encephalopathy: because of respiratory failure caused by brain dysfunction, patients can show a series of neuropsychiatric symptoms, such as directional, memory disorders, confusion, headache, drowsiness, coma and so on.ARDS (acute respiratory distress syndrome): respiratory dysfunction caused by alveolar capillary membrane injury caused by various reasons and the occurrence of acute respiratory failure syndrome clinical characteristics, is characterized by progressive dyspnea and hypoxemia.Hepatic encephalopathy: neuropsychiatric syndrome secondary to severe liver disease.False neurotransmitter: phenylethanolamine and octopamine in chemical structure and normal neurotransmitter norepinephrine and dopamine are similar, but can not complete the authenticity of neurotransmitter function, known as false neurotransmitter.Hepatorenal syndrome: acute renal tubular necrosis associated with functional renal failure and severe hepatitis in decompensated cirrhosis.Acute renal failure due to GFR decreased rapidly, or renal tubular degeneration and necrosis in a pathological process caused by acute severe, often oliguria, azotemia, hyperkalemia, metabolic acidosis and water intoxication syndrome.Chronic renal failure:Any disease of renal unit destruction, in the months and years or longer after the remaining nephron cannot fully remove metabolic waste and environment, thus to maintain the constant in the gradual emergence of metabolic waste retention and water electrolyte and acid-base balance disorders and renal endocrine dysfunction.The levels of non protein nitrogen (NPN) in blood, including uremia, creatinine, uric acid, and so on, are called azotemia. The NPN in normal blood is 25~35mg%, and the urea nitrogen is 10-15mg%.Renal hypertension: hypertension caused by renal parenchymal disease is called renal hypertension.Uremia: refers to acute or chronic renal failure to severe stage, metabolites and toxins accumulate in the body, water, electrolyte and acid-base balance disorders and some endocrine disorders caused by a series of systemic function and metabolic disorder syndrome.Two, Jane answer1. briefly describe the diagnostic criteria for brain deathAccording to the determination of brain death is the irreversible coma and brain response; second, stop breathing for 15 minutes, artificial respiration still no spontaneous breathing; the cranial nerve reflex; the pupil or fixed; the brain waves disappeared; the complete cessation of cerebral blood circulation (cerebral angiography).2. which type of dehydration is prone to loss of fluid shock? Why?Hyponatremia with low volume (hypotonic glue) is liable to cause fluid shock. (1) the extracellular fluid Bian through thepressure drop, no thirst, drinking water reducing. (2) the extracellular fluid Bian through pressure reduction, ADH reflex secretion decreased, no significant decrease in urine volume.(3) the extracellular fluid transferred to the intracellular fluid, and the extracellular fluid decreased further.3. to analyze the influence of water intoxication on the body.Extracellular fluid was diluted due to excessive water, so the blood sodium concentration decreased and osmotic pressure decreased. In addition, the kidney can not discharge too much water in time, the water is transferred to the relatively high osmotic pressure cells, causing edema. The result is that both the intracellular and external fluid volume are increased, and the osmotic pressure is decreased. Because the cell liquid capacity greater than the extracellular fluid retention capacity, so most of the moisture accumulation in the cells, therefore in mild water intoxication, interstitial water retention degree is still not enough to cause recessive edema of the concave. Acute water intoxication, the nerve cells in the brain edema and intracranial pressure, the cerebral symptoms appeared earliest and prominent, can occur in various neuropsychiatric symptoms, such as gaze, aphasia, confusion, lethargy, irritability and other directional arrhythmia, and papilloedema, severe cases can occur due to cerebral hernia caused by respiratory and cardiac arrest patients with mild, chronic or water poisoning is slow, symptoms are often not obvious, many covered by the symptoms and signs of primary disease, can have drowsiness, headache, nausea, vomiting,muscle spasms and pain symptoms such as weak and feeble.4. to discuss the mechanism of edema caused by imbalance of fluid exchange inside and outside the blood vessel.The force that drives the flow out of the intravascular fluid is the average effective hydrostatic pressure. The force that causes the fluid to flow back into the capillaries is effective colloid osmotic pressure. Normally, the tissue fluid is slightly larger than the reflux. Lymph reflux, tissue fluid reflux, the remaining part of the lymphatic system through the backflow into the blood circulation, normal adults in quiet state, enzyme hours about 120ml liquid through the lymphatic system into the blood circulation. The interstitial fluid increased hydrostatic pressure, and the rate of lymph formation was accelerated. In addition, the permeability of the lymphatic wall is higher and the protein is easy to pass. Therefore, lymph reflux can not only send a little more of the tissue fluid back into the body, but also the proteins that leak out of the capillaries, and the large molecules produced by cell metabolism absorb the circulation of the body. One or more of these factors at the same time or one after another disorders may be an important cause of edema.5. hypokalemia and hyperkalemia can cause muscle paralysis. What is the mechanism of this?Hypokalemia is mainly due to hyperpolarized block. The ratio of [K+ /[K+]e] the increase of hypokalemia, and muscle cell negative resting potential, the resting potential and threshold potential interval increases, cell excitability anddecreased, even not serious when excited, i.e. cells in the hyperpolarized state block. Hyperkalemia results in inactivation of the fast sodium channel because of the small resting potential of the skeletal muscle and is unable to be excited by extracellular depolarization.6. what kinds of acid-base disorders are caused by severe vomiting? To analyze the mechanism of its occurrence.Severe vomiting easily leads to metabolic alkalosis:H+ lost the gastric juice, the digestive tract of HCO3- H+ is not neutralized and absorbed into the blood; the loss of Cl- in gastric juice, can cause hypochloremic alkalisis; K+ lost the gastric juice, can cause hypokalemic alkalosis; the loss caused by a large amount of gastric juice, effective circulating blood volume reduction, secondary aldehyde solid ketone the increase caused by metabolic alkalosis.7. what types of acid-base disturbances can occur in the oliguria stage of acute renal failure? Why? What are the changes in the acid-base balance index?Can occur because of metabolic acidosis, renal function and acid alkali, in severe renal failure, can not be fixed in acid by urinary excretion, especially sulfuric acid and phosphoric acid accumulation in the body, resulting in the increase of H+ concentration HCO3- concentration decreased, due to reduced HCO3-, so AB, SB and BB significantly decreased. Negative BE increased, PH decreased by Paco2 secondary respiratory compensation, down AB<SB.8. what type of hypoxia can be caused by hemorrhagic shock?.Hemorrhagic shock, due to a large number of blood loss and lack of tissue blood, resulting in inadequate oxygen supply, can lead to circulatory hypoxia.9. what kind of hypoxia can pulmonary edema cause? Its hypoxia mechanism?Can cause hypoxic hypoxia, due to pulmonary edema, ventilation function of fertilizer limited caused by alveolar PO2 decreased, pulmonary ventilation dysfunction by alveolar diffuse into the blood oxygen reduction, PaO2 and lack of oxygen, caused by hypoxic hypoxia.10. to analyze the mechanism of red blood cell growth during chronic hypoxia.When the number of red blood cells in chronic hypoxia is mainly due to the increase in renal production and release of erythropoietin EPO; hypoxia can increase the activity of HIF-1 in cytoplasm, HIF-1 gene and EPO 3 enhancer binding, enhanced the expression of EPO gene, the EPO increased, the molecular weight of EPO was 34000 of the egg white sugar, can promote stem cell the original red blood cell differentiation, and promote the differentiation, proliferation and maturation, accelerate the synthesis of hemoglobin, the bone marrow reticulocyte and red blood cells released into the blood.11. try to describe the mechanism of shortness of breath inpeople on the upper plateau.The air in the plateau is thin and low in oxygen,At the beginning of the plateau, hypoxia induced PAO2 below 60mmHg and stimulated the peripheral chemoreceptor of the carotid body and the aortic body. The impulses were introduced into the medulla via the sinus nerve and the vagus nerve, which caused the respiration to accelerate gradually.12. can arterial blood pressure be used as a marker for the occurrence of shock? Why?No, because the shock early sympathoadrenomedullary excitement, heart rate, contractility increased, blood transfusion and infusion through their own, as well as increased renal reabsorption of sodium and water, increase the turn output, so that the increased cardiac output, plus the peripheral resistance increased, so the blood pressure was not obvious.13. to describe the characteristics and compensatory significance of microcirculatory changes in early stage of shock.Is the early stage of shock shock compensatory, the sympathetic nervous excitement, increased catecholamine, some organs of small vascular contraction or spasm, especially micro artery, after arterioles and precapillary sphincter contraction, the precapillary resistance increased, capillary closure, true capillary network reduced blood flow, blood flow slows down; beta adrenergic receptor the stimulated arteriovenousanastomoses are open, blood through the direct pathway and open the arteriovenous anastomosis reflux, microcirculation of non nutritive blood flow increase, reduce nutrient flow, severe hypoxic ischemic tissue. The above changes of microcirculation, on the one hand, cause ischemia and hypoxia of organs such as skin, abdomen, viscera and kidneys, on the other hand, they have compensatory significance to the whole. The main manifestations are: blood redistribution, autotransfusion, and self infusion.14. the mechanism of microcirculatory changes in shock stage II.The mechanism of microcirculatory changes in progressive stage is related to the effects of prolonged microvascular contraction and ischemia, hypoxia, acidosis, and various humoral factors.Acidosis: hypoxia leads to the decrease of tissue oxygen partial pressure, accumulation of CO2 and lactic acid and acidosis. Acidosis causes a decrease in the responsiveness of vascular smooth muscle to catecholamines and causes vasodilation.The local vasodilator metabolites increased: long-term ischemia and hypoxia, acidosis stimulates the release of histamine from mast cells increased, ATP decomposition products of adenosine accumulation, kinins generation increases, can cause vascular smooth muscle relaxation and telangiectasia.The changes of blood rheology: shock progression blood flow decreased obviously, micro slow blood flow in erythrocyte aggregation and easy; the effect of histamine on capillary permeability, plasma extravasation, blood viscosity increased; perfusion pressure decreased, resulting in leukocyte rolling, adhesion and adhesion to endothelial cells, blood blocked postcapillary resistance increased.IV: the role of endotoxin: the relaxation of vascular smooth muscle, resulting in persistent hypotension.15. what is the most common cause of multiple organ dysfunction syndrome (MODS)? Its pathogenesis?80% of the MODS patients had significant shock when they entered the hospital.Infectious causes, such as sepsis and severe infection, can affect approximately 70% of MODS, especially sepsis caused by severe infections.Non infectious causes such as major surgery and severe trauma, major surgery and severe trauma, whether or not infections are pure, can occur in MODS.Pathogenesis: (1) the general inflammatory response is out of control. Promoting the imbalance between anti-inflammatory and anti-inflammatory mediators. Other factors that cause organ dysfunction: organ microcirculation perfusion disorder, high metabolic state, ischemia-reperfusion injury.What is the mechanism of 16.DIC?The release of tissue factor, the activation of exogenous coagulation system, the initiation of blood coagulation system, the damage of vascular endothelial cells, the imbalance of coagulation and anticoagulant regulation, the destruction of blood cells, the activation of platelets, and the introduction of procoagulant substances into the blood.What is the mechanism by which 17.DIC leads to shock?Because of the large amount of micro thrombus in blood vessel, the microcirculation is blocked and the blood volume is reduced obviously. Extensive bleeding can reduce the volume of blood. The injury of cardiac muscle leads to decrease of cardiac output. The activation of coagulation factor XII may activate the kallikrein system, complement system and fibrinolytic system, and produce some vasoactive substances, such as bradykinin and complement components. The complement component can make the basophils and mast cells release histamine, etc. the peptide and histamine can relax the microvascular smooth muscle, increase the permeability, reduce the peripheral resistance and reduce the blood volume. Some components of FDP can enhance the action of histamine, bradykinin and promote the expansion of microvessels.18. try to explain the compensatory response of the heart when the heart function is incomplete.Heart rate increased, heart tension dilated, myocardial contraction increased, ventricular remodeling19. cardiac insufficiency after the type of compensatory cardiac hypertrophy and its mechanism, sarcomere replication.Hypertrophy of the heart can be caused by a variety of reasons. When partial myocardial cells are lost, reactive myocardial hypertrophy may occur in the residual myocardium. Prolonged overload can cause excessive cardiac hypertrophy,According to the cause of overload and cardiac reaction of different forms can be divided into overload cardiac hypertrophy: concentric hypertrophy, cardiac function in long-term excessive load pressure, systolic wall tension increase myocardial sarcomere parallel type hyperplasia, thickening of myocardial cells. Eccentric hypertrophy, heart in the long-term excessive load capacity, diastolic wall tension increase myocardial sarcomere was series hyperplasia, myocardial cell growth, ventricular volume increases; while the heart enlargement and systolic wall stress increases, and thus stimulate the proliferation of sarcomere parallel.20. briefly describe the mechanism and significance of heart rate reduction during heart failure.The mechanism of heart rate is: due to decreased cardiac output, heart rate caused by the intracardiac residual blood volume is increased; reduce the heart pump blood, ventricular end diastolic volume and pressure, can stimulate the right atrium and vena cava volumereceptor, via vagal afferent fibers in the vagus nerve to pivot, inhibition, sympathetic stimulation. If the combined hypoxia can stimulate the aortic body and carotidbody chemoreceptor, reflex excitability causes heart rate to accelerate. Significance: cardiac output is the product of stroke volume and heart rate, in a certain range, can improve the heart rate, cardiac output, and can improve the diastolic blood pressure, blood perfusion to the coronary artery, to maintain arterial blood pressure, which is of positive significance to the blood supply to vital organs.21. what is the mechanism of dyspnea caused by heart failure? What types of dyspnea do you have?Mechanism: lung congestion and pulmonary edema lead to lower lung compliance. To breathe the same amount of air, it is necessary to increase the work done by the respiratory muscle and consume more energy, so the patient feels labored. The bronchial mucosal hyperemia, swelling and airway secretions lead to airway resistance increases; the pulmonary capillary pressure and interstitial edema of pulmonary interstitial pulmonary capillary pressure increased, stimulation of fat receptors, causing reflex rapid shallow breathing. Types include exertional dyspnea, dyspnea, and paroxysmal nocturnal dyspnea.22. the severe hypokalemia (or excessive anesthetics, sedatives, hypnotics, severe pneumothorax, pleural effusion, obstruction of trachea, bronchial asthma, chronic bronchitis) the pathogenesis of respiratory failure caused by.The main effects of hypokalemia on the body is the membrane potential caused by the abnormal effect of nerve muscle, muscle relaxation of skeletal muscle weakness and even paralysis,leading to respiratory muscle contraction diastolic dysfunction caused by restrictive ventilation due to insufficient pulmonary dysfunction, which is outside the alveolar gas and gas exchange in extracellular potassium ion concentration in cell metabolism disorder caused by the disturbance of acid-base balance disorders, hypokalemia decreased, intracellular potassium concentration gradient transfer to the outside of the cell and extracellular hydrogen ion transfer to the cells increased, the hydrogen potassium exchange; the renal ammonia (hydrogen ions).23. to discuss the pathogenesis of pulmonary heart disease.The alveolar hypoxia and CO2 retention caused by blood H+ concentration is too high, can cause pulmonary arteriolar constriction, the pulmonary arterial pressure increased, thereby increasing the right ventricular afterload; pulmonary arteriole contraction and hypoxia can cause non muscular arterioles in muscle, pulmonary vascular smooth muscle cells to fibroblast cell hyperplasia, collagen and elastin synthesis increase, lead to pulmonary vascular wall thickening and lumen narrowing, hardening, resulting in chronic pulmonary hypertension lasting and stable due to the long-term hypoxia; compensatory polycythemia can increase blood viscosity, will also increase the resistance of pulmonary blood flow and increased right heart load; and some abdominal diseases such as pulmonary arteritis, small the destruction of a large number of pulmonary capillary and pulmonary embolism can be a cause of pulmonary hypertension; the hypoxia and acidosis family cardiac contractility and dyspnea, Forced expiratory intrathoracic pressure can cause abnormal increase of cardiaccompression effect of cardiac diastolic function, abnormal inspiratory intrathoracic pressure is reduced, the negative pressure outside the heart increases, increased right ventricular systolic load to right heart failure.24. to discuss the pathogenesis of pulmonary encephalopathyEffects of hypoxia, acidosis and hypercapnia on cerebral blood vessels:1, hypoxia and acidosis to cerebral vascular dilation; 2, hypoxia and acidosis leads to vascular endothelial injury: one is to increase vascular permeability, aggravate brain edema, while promoting intravascular coagulation; 3, hypoxia and acidosis reduced the formation of ATP: dysfunction of sodium pump, cell edema, cerebral vascular compression increased intracranial pressure, intracranial pressure, cerebral vascular compression, increased hypoxia, and forming a vicious spiral.Two. The effects of hypoxia, acidosis and hypercapnia on neurons:1, on the one hand, hypoxia can directly inhibit brain function, on the other hand can cause dysfunction of sodium pump, make the brain edema, increased intracranial pressure; 2, hypercapnia easily lead to intracellular acidosis, on the one hand, the glutamic acid decarboxylase activity increased, the increasing production of GABA, inhibit the function of central nervous system,On the other hand, it can enhance phospholipase activity, decompose membrane phospholipids, dissolve lysosomes, and aggravate the damage of nerve cells.What is the cause of elevated blood ammonia in 25. hepatic encephalopathy? What are the toxic effects of ammonia intoxication on the brain?.The reasons for the increase of blood ammonia include: the decrease of urea synthesis and the lack of ammonia clearance. Toxicity: 1, ammonia to neurotransmitters in the brain changes, brain cell energy metabolism and ammonia the interference effect on the nerve cell membrane pump: NA-K interference on the nerve cell membrane; competition of K ion and ion distribution of membrane.26. what are the metabolic changes in acute renal failure and oliguria? Explain its mechanism.The change of urine: oliguria, anuria, low proportion of urine, hematuria, proteinuria, urinary tube; functional ARF, renal function is not damaged, the oliguria is mainly due to GFR significantly reduced by, and the organic ARF and glomerular and renal tubular dysfunction.Water intoxication: ARF, for reasons of oliguria, catabolism caused by increased intake of water, in the water too much, resulting in water retention, dilutional hyponatremia and cell edema at.The hyperkalemia: potassium with the urine reduced urine volume;。
最完整病理学名词解释及问大全带答案
（带答案）病理学名词解释及问答题大全四、问答题0.4.01举例说明病理学在医学中的地位0.4.02简述病理学常用研究方法的应用及其目的0.4.03简述病理学的发展史一、名词解释0.1.01病理学(pathology)0.1.02病理解剖学(pathologic anatomy or anatomical pathology)0.1.03病因学(etiology)0.1.04发病机制(pathogenesis)0.1.05病理变化(pathologic changes)0.1.06尸体解剖(autopsy)0.1.07活体组织检查(biopsy)0.1.08细胞学(cytology)0.1.09组织培养(tissue culture)0.1.10组织化学(histochemistry)0.1.11分子病理学(molecular pathology)0.1.12免疫组织化学(immunohistochemistry)0.1.13基因诊断(gene diagnosis)答案一、名词解释（此处仅列出答案要点）0.1.01①一门医学基础学科；②研究疾病的病因、发病机制、病理变化（形态、代谢和功能变化）；③目的：认识疾病的本质和发生发展规律，为防病治病提供理论基础和实践依据。
0.1.02①病理学的重要组成部分；②从形态学角度研究疾病；③研究病变器官的代谢和功能改变及临床表现；④研究病因学和发病学。
0.1.03研究疾病的病因、发生条件的一门科学。
0.1.04①即发病学；②在原始病因和发生条件的作用下，疾病发生发展的具体环节、机制过程。
0.1.05①在病原因子和机体反应功能的相互作用下；②疾病过程中脏器和组织功能、代谢和结构的变化。
0.1.06①一种病理学的基本研究方法；②对死者遗体进行病理剖验；③目的：确定诊断、查明死亡原因，提高临床医疗水平；及时发现传染病和新的疾病；为科研和教学积累资料和标本。
0.1.07①患者机体的病变组织；②组织获取方法：局部切除、钳取、穿刺针吸以及搔刮、摘除等；③目的：研究疾病、诊断疾病。
病理生理学名词解释简答论述大题
病理生理学名解1.健康：一种躯体上、精神上和社会适应上的完好状态，而不仅是没有疾病或衰弱现象。
〔5〕2.疾病：在一定病因作用下，机体稳态发生紊乱而导致的异常生命活动过程。
〔6〕3.衰老：又称老化，是机体正常功能随年龄增长而逐渐减退的不可逆过程。
〔6〕4.诱因：加强病因作用而促进疾病发生开展的因素。
〔7〕5.病因:引起疾病必不可少的、决定疾病特异性的因素。
〔7〕6.危险因素：与某一疾病具有明显相关，但尚分不清是原因还是条件因素。
〔8〕7.脑死亡：全脑功能不可逆的永久性丧失以及机体作为一个整体功能的永久性停止。
〔11〕8等渗性脱水：体液容量减少，按正常血浆中的浓度比例丧失水和钠，血清钠浓度仍维持在130~150 mmol/L及血浆渗透压仍维持在280~310 mmol/L正常水平的病理过程。
〔19〕9.高渗性脱水：体液容量减少，以失水多于失钠，血清钠浓度＞150 mmol/L及血浆渗透压＞310 mOsm/L 为主要特征的病理过程。
〔20〕10.低渗性脱水：体液容量减少，以失纳多于失水，血清钠浓度＜130 mmol/L及血浆渗透压＜280 mOsm/L为主要特征的病理过程。
〔21〕11.水肿：过多的液体在组织间隙或体腔中积聚的病理过程，它是多种疾病的临床体征。
〔22〕12..水中毒：水在体内潴留，并伴有包括低钠血症、脑神经细胞水肿等一系列病症和体征的病理过程。
〔26〕13.盐中毒：又称高血钠性细胞外液溶液增多，是体内钠总量和血钠含量增高伴有细胞外液增多的病理过程。
〔27〕14.低钾血症：血清钾浓度低于3.5mmol/L。
高钾血症：血清钾浓度高于5.5mmol/L〔33〕15.酸碱平衡紊乱：病理情况下，机体出现酸或碱超量负荷、严重缺乏或调节机制障碍，而导致机体内环境酸碱度的稳定性被破坏过程。
〔43〕16.实际碳酸氢盐：隔绝空气的血液标本，在实际PaCO2、血氧饱和度及体温条件下，所测得的血浆HCO3-含量。
病理生理学名词解释简答题库
病理生理学名词解释简答题库【病理生理学pathophysiology】【基本病理过程fundamental pathological process】【健康】【疾病】【脑死亡brain death】【水肿edema】【水中毒water intoxication】【低钾血症hypokalemia】【高钾血症hyperkalemia】【呼吸性酸中毒Respiratory acidosis】【代谢性酸中毒Metabolic acidosis】【标准碳酸氢盐SB】【血氧分压Partial Pressure of Oxygen,PO2】【血氧容量oxygen binding capacity,CO2max】【血氧含量Oxygen Content，CO2】【血氧饱和度oxygen saturation of hemoglobin，SO2】【动静脉氧含量差CaO2－CvO2】【缺氧Hypoxia】【循环性缺氧（circulatory hypoxia）】【低张性缺氧(hypotonic hypoxia)】【呼吸性缺氧repiratory hypoxia】【组织性缺氧Histogenous Hypoxia】【血液性缺氧Hemic Hypoxia】【发绀cyanosis】【功能性分流functional shunt】【解剖分流anatomic shunt】【阴离子间隙anion gap，AG】【应激Stress】【应激原Stressor】【应激性溃疡Stress ulcer，SU】【休克shock】【休克肺shock lung】【肺性脑病pulmonary encephalopathy】【肝性脑病hepatic encephalopathy，HE】【全身炎症反应综合征systemic inflammatory response syndrome，SIRS】【多器官功能障碍综合症multiple organ dysfunction syndrome，MODS】【肺源性心脏病】【急性肾功能衰竭acute renal failure,ARF】【慢性肾功能衰竭Chronic Renal Failure，CRF】【氮质血症azotemia】【假性神经递质（false neurotransmitter)】【综合征syndrome】【跨细胞液(第三间隙液)】【高渗性脱水hypertonic dehydration】【低渗性脱水Hypotonic dehydration】【等渗性脱水Isotonic dehydration】【代谢性碱中毒Metabolic alkalosis】【蓝斑-交感-肾上腺髓质系统（locus ceruleus-norepinephrine/sympatheticadrenal medullatty system，LC/NE）】【蓝斑】【热休克反应(heat shock response,HSR)】【热休克蛋白Heat shock protein,Hsp】【急性期反应（acute phase response,APR）】【全身适应综合征General adaptation syndrome，GAS【急性呼吸窘迫综合征acute respiratory distress syndrome，ARDS】【肝功能不全Hepatic insufficiency】【肝功能衰竭Hepatic failure】【尿毒症uremia】【心室重塑ventricular remodeling】【心肌肥大Myocardial hypertrophy】【心功能不全（cardiac insufficiency）】【劳力性呼吸困难dyspnea on exertion】【夜间阵发性呼吸困难paroxysmal nocturnal dyspnea】【端坐呼吸orthopnea】【急性肺水肿】【肝肾综合征hepatorenal syndrome，HRS】【呼吸衰竭respiratory failure】1、疾病发生发展的一般规律？试就其中一个规律举例说明？2、水、钠代谢障碍的分类?3、低钾血症对机体的影响？4、高血钾症对机体的影响？5、低血钾症和严重高血钾症均可导致骨骼肌弛缓性麻痹，简述其机制有何异同？6、低钾血症对心肌生理特性的影响7、低钾血症的心电图变化8、高渗性脱水的原因和机制，对机体的影响？9、低渗性脱水的原因和机制对机体的影响？10、等渗性脱水的原因和对机体的影响？11、低渗性脱水早期尿量不减少，晚期尿量减少机制。
病理生理学 名词解释 及大题
病理生理学pathophysiology：是一门研究疾病发生、发展、转归的规律和机制的科学。
病理过程pathological process：多种疾病过程中出现的共同的功能、代谢和形态的病理变化。
疾病：在致病因素的损伤与机体的抗损伤作用下，因自稳调节紊乱而发生的异常生命活动过程。
致病因素etiological factors ：能够引起某一疾病并决定疾病特异性的因素。
诱因(predisposing factor)：作用于病因或机体促进疾病发生发展的因素。
恶性循环（vicious cycle）：在某些疾病因果交替的发展过程中，几种变化互为因果，构成一个环式运动，每一次循环都使病情加重，称恶性循环。
完全康复（complete recovery）是指病因去除后，患病机体的损伤和抗损伤反应完全消失、形态结构损伤完全修复、机体功能和代谢完全恢复到正常状态，以及临床症状和体征完全消退。
不完全康复（incomplete recovery）是指原始病因消除后，患病机体的损伤性变化得以控制，但机体内仍存在病理变化，只是机体通过代偿反应维持相对正常的生命活动。
脑死亡（brain death）是指以脑干或脑干以上全脑不可逆转的永久性地功能丧失，使得机体作为一个整体功能的永久停止。
脱水dehydration：钠水代谢紊乱造成体液容量的明显减少导致机体功能和代谢紊乱的病理过程。
脱水热：由于从皮肤蒸发的水分减少，使散热受到影响，从而导致体温升高，称之为脱水热。
脱水征：因组织间液量减少，临床上出现皮肤弹性减退、眼窝下陷，婴幼儿囟门凹陷等体征。
水肿edema：过多的液体在组织间隙或体腔内积聚称为水肿。
隐性水肿（recessive edema）指全身水肿病人的组织液增多小于原体重的10%，增多的液体能被组织间隙中的胶状物完全吸附，故无游离液体存在，因此局部按压无凹陷出现。
凹陷性水肿（recessive edema）指全身水肿病人的组织液增多超过原体重的10%，增多的液体不能被组织间隙中的胶状物完全吸附，故有游离液体存在，皮肤肿胀，弹性差，皱纹变浅，按压有凹陷。
病理生理学题库及答案——水、电解质代谢紊乱
病理生理学第十四章水、电解质代谢紊乱一、名词解释1.低钠血症2.高钠血症3、低容量性低钠血症4.低容量性高钠血症5.高容量性低钠血症6.积水7.水肿8.钠水潴留9.凹隐性水肿10.脑水肿11.低钾血症12.高钾血症13.反常性酸性尿14.反常性碱性尿二、填空题1.溶液的渗透压取决于溶质的分子或离子的_____ ，体液中起渗透作用的溶质主要是_____。
2.通常血浆渗透压在_____mmol/L，在此范围内称_____。
3.低钠血症是指血清钠浓度_____，高钠血症是指血清钠浓度_____。
4.低渗性脱水的特点是失Na+_____失水，伴有细胞外液量_____。
5.低容量性低钠血症患者血清Na+浓度_____，血浆渗透压_____。
6.高渗性脱水时血清钠浓度_____，低容量性高钠血症又称_____。
7.高渗性脱水的特点是失水_____失钠，细胞外液和细胞内液量是_____。
8.水肿液含有血浆的全部晶体成分，根据蛋白含量的不同分为_____和_____。
9.漏出液的相对密度低于_____，蛋白质含量低于_____。
10.渗出液的相对密度高于_____，蛋白质含量可达_____。
11心性水肿首先出现在_____部位，而肝性水肿以_____为多见。
12低钾血症是指血清钾浓度低于_____，高钾血症是指血清钾浓度大于_____。
13低钾血症时心肌兴奋性_____，传导性_____。
14.低钾血症时心肌自律性_____，收缩性_____。
15.低钾血症时心电图的典型表现为_____波低平，_____波增高。
16轻度高钾血症时，心肌兴奋性_____，而严重高钾血症时心肌兴奋性_____。
17.高钾血症时，心肌自律性_____，收缩性_____。
18.高钾血症可出现各种各样的心律失常，特别是可出现一些致死性的心律失常如_____、_____。
19.高钾血症时骨骼肌的兴奋性随血清钾浓度逐步升高可经历先_____后_____的过程。
病理生理学题库-名词解释
病理过程（pathological process）存在于不同疾病中的共同的成套的功能﹑代谢与形态结构的变化。
1.疾病（disease）[答案]疾病是机体在一定病因的损害下，因机体自稳调节紊乱而发生的异常生命活动过程.3.病因（cause）[答案]又称原因，是引起某种疾病的因素，又决定该疾病的特异性，是疾病发生必不可缺少的因素。
9.脑死亡（brain death）[答案]是指包括大脑和脑干的全脑死亡，意味着机体作为一个整体的功能永久停止，这是判断脑死亡的标志。
1. 低渗性脱水[答案]特点是失Na+多于失水，血清Na+浓度<130mmol/L伴有细胞外液量减少。
2.水中毒[答案]特点是血清Na+浓度<130mmol/L，血浆渗透压<280mmol/L，但体钠总量正常或增多，患者有水潴留使体液量明显增多。
3. 高渗性脱水[答案]特点是失水多于失钠，血清Na+浓度>150mmol/L，血浆渗透压>310mmol/L，细胞外液和细胞内液均减少。
4.水肿（edema）(04护本、检验，易而无区别，0.118，0.3)（0.237，0.367，03临床）[答案]过多的液体在组织间隙或体腔内积聚。
5. 显性水肿(凹陷性水肿)[答案]皮下组织内有过多的游离液体积聚时，用手指按压出现凹陷的水肿。
6.隐性水肿（recessive edema）[答案]过多的液体在组织间隙积聚，但未出现凹陷特征的水肿，此时组织液明显增多，可达体重的10%。
7.低钾血症（hypokalemia）[答案]指血清钾浓度低于3.5mmol/L。
8.高钾血症（hyperkalemia）[答案]指血清钾浓度大于5.5mmol/L。
1.代谢性酸中毒(metabolic acidosis)[答案]由于血浆HCO3-原发性减少所引起的pH值降低。
2.AG增高型代谢性酸中毒(metabolic acidosis with increased AG)[答案]指血浆中不含氯的固定酸浓度增加时AG增大、血氯正常的代谢性酸中毒。
病理学名词解释及问答题总结(第十三章)
病理学名词解释及问答题总结（第十三章）内分泌系统疾病内分泌系统（endocrine system）包括内分泌腺、内分泌组织（胰岛）和散在于各系统或组织内的内分泌细胞。
远距离分泌（telecrine）为大多数激素经血液运输至远距离的靶细胞或组织而发挥作用。
旁分泌（paracrine）某些激素不经血液运输，仅由组织液扩散而作用于邻近细胞。
自分泌（autocrine）有的激素作用于分泌激素的细胞本身。
胞内分泌（endocellular secretion）内分泌细胞的信息物质不分泌至胞外，原位作用于该细胞质内的细胞器上。
按激素的化学性质可分为含氮激素和类固醇激素。
含氮激素主要在粗面内质网和高尔基复合体内合成，其分泌颗粒有包膜。
类固醇激素在滑面内质网内合成，分泌颗粒无包膜。
第一节垂体疾病垂体位于蝶鞍垂体窝内，由神经垂体和腺垂体组成。
神经垂体分为神经部和漏斗部，腺垂体又分为远侧部、中间部、结节部。
远侧部最大，又称为垂体前叶，神经部和中间部合成后叶。
一．下丘脑及垂体后叶疾病（一）尿崩症（diabetes insipidus）由于抗利尿激素（ADH）缺乏或减少而出现多尿、低比重尿、烦渴和多饮等临床症状。
病因和分类：①因垂体后叶释放ADH 不足引起，称为垂体性尿崩症；②因肾小管对血内正常ADH水平缺乏反应，则称为肾性尿崩症；③因下丘脑-垂体后叶轴的肿瘤、外伤、感染等引起，称为继发性尿崩症；④原因不明者，称特发性或原发性尿崩症。
（二）性早熟症（precocious puberty）因中枢神经系统疾病（脑肿瘤、脑积水）或遗传异常而使下丘脑-垂体过早分泌释放促性腺激素所致，表现为女孩6-8岁，男孩8-10岁前出现性发育。
二．垂体前叶功能亢进与低下（腺垂体远侧部）垂体前叶功能亢进（hyperpituitarism）是前叶的某一种或多种激素分泌增加，一般由前叶功能性肿瘤引起，少数由下丘脑作用或其靶器官反馈抑制作用消失所致。
(整理)病理生理学重要章节精题包括名词解释、选择题、问答题
选择题绪论1. 病理生理学是研究(c )疾病发生发展规律和机制的科学2. 疾病概论主要论述( c)疾病具有普遍性的机制3. 病理生理学研究疾病的最主要方法是动物实验第三章7．水肿首先出现于身体低垂部,可能是(c )A.肾炎性水肿B.肾病性水肿C.心性水肿D.肝性水肿E.肺水肿12．临床上对伴有低容量性的低钠血症原则上给予等渗氯化钠溶液13．尿崩症、盛暑行军时大量出汗可发生(b )A.等渗性脱水B.低容量性低钠血症C.低容量性高钠血症15．低容量性高钠血症患者的处理原则是补充. 先5%葡萄糖液,后0.9%NaCl液第四章一、选择题6．血液中挥发酸的缓冲主要靠(c ) A.血浆HCO3ˉ B.红细胞HCO3ˉ C.HbO2及Hb D.磷酸盐 E.血浆蛋白9．能直接反映血液中一切具有缓冲作用的负离子碱的总和的指标是( d) A.PaCO2B.实际碳酸氢盐（AB）C.标准碳酸氢盐（SB）D.缓冲碱（BB）E.碱剩余（BE）17．治疗代酸的首选药物是.乳酸钠34．肾小管酸中毒引起的代谢性酸中毒，下列哪项不存在( ) A.血K+升高B.AG升高C.PaCO2下降D.BE负值增大E.Cl－增高第五章一、选择题1．影响动脉血氧分压高低的主要因素是(d )D．肺呼吸功能和吸入气分压2．影响动脉血氧含量的主要因素是(d )D．动脉血氧分压和血氧容量4．检查动-静脉血氧含量差主要反映的是(e )组织摄取和利用氧的能力7．易引起血液性缺氧的原因是( b) A．氰化物中毒组织性缺氧B．亚硝酸盐中毒C．硫化物中毒D．砒霜中毒E．甲醇中毒10．引起循环性缺氧的疾病有( c)动脉痉挛或受压、动脉硬化、血管炎、血栓形成和栓塞、心力衰竭休克11．砒霜中毒导致缺氧的机制是(d ) A．丙酮酸脱氢酶合成减少B．线粒体损伤C．形成高铁血红蛋白D．抑制细胞色素氧化酶E．血红蛋白与氧亲和力增高12．氰化物中毒时血氧变化的特征是(e )动-静脉血氧含量差降低16．下列哪项不是缺氧引起的循环系统的代偿反应(c ) A．心率加快 B．心肌收缩力加强C．心、脑、肺血管扩张收缩D．静脉回流量增加E．毛细血管增生19．慢性缺氧时红细胞增多的机制是(e ) A．腹腔内脏血管收缩B．肝脾储血释放C．红细胞破坏减少D．肝脏促红细胞生成素增多E．骨髓造血加强第十一章一、单择题1．休克是(b ) A．以血压下降为主要特征的病理过程B．以急性微循环功能障碍为主要特征的病理过程C．心输出量降低引起的循环衰竭D．外周血管紧张性降低引起的周围循环衰竭E．机体应激反应能力降低引起的病理过程2．低血容量性休克的典型表现不包括( ) A．中心静脉压降低B．心输出量降低C．动脉血压降低D．肺动脉楔压增高E．总外周阻力增高3．下列哪项不属于高排低阻型休克的特点( ) A．总外周阻力降低B．心输出量增高C．脉压增大D．皮肤温度增高E．动-静脉吻合支关闭4．下列哪项不是休克Ⅰ期微循环的变化(d ) A．微动脉、后微动脉收缩B．动-静脉吻合支收缩C．毛细血管前括约肌收缩D．真毛细血管关闭E．少灌少流，灌少于流5．休克Ⅰ期“自身输血”主要是指( d) A．动-静脉吻合支开放，回心血量增加B．醛固酮增多，钠水重吸收增加C．抗利尿激素增多，重吸收水增加D．容量血管收缩，回心血量增加E．缺血缺氧使红细胞生成增多6．休克Ⅰ期“自身输液”主要是指( b) A．容量血管收缩，回心血量增加B．毛细血管内压降低，组织液回流增多C．醛固酮增多，钠水重吸收增加D．抗利尿激素增多，重吸收水增加E．动-静脉吻合支开放，回心血量增加20．休克初期发生的急性肾功能衰竭是由于( a) A．肾灌流不足B．持续性肾缺血C．肾毒素作用D．急性肾小管坏死E．输尿管阻塞二、问答题 1.休克Ⅰ期微循环改变有何代偿意义？第十二章弥散性血管内凝血一、单择题1.在启动凝血过程中起主要作用的是(c )A.血小板B.FⅦC.FⅫD.FⅢE.凝血酶20.DIC患者最初常表现为( b)A.少尿B.出血C.呼吸困难D.贫血E.嗜睡23.DIC引起的贫血属于( ) A.再生障碍性贫血 B.失血性贫血 C.中毒性贫血 D.溶血性贫血 E.缺铁性贫血24.DIC最主要的病理生理学特征是( ) A.大量微血栓形成 B.凝血功能失常 C.纤溶过程亢进 D.凝血物质大量被消耗 E.溶血性贫血25.引起微血管病性溶血性贫血发生的主要因素是(b )A.微血管内皮细胞大量受损B.纤维蛋白丝在微血管内形成细网C.小血管内血流淤滞D.微血管内大量微血栓形成E.小血管强烈收缩27.DIC时，血液凝固性表现为(c ) A.凝固性增高 B.凝固性降低 C.凝固性先增高后降低 D.凝固性先降低后增高 E.凝固性无明显变化第十三章一、选择题A型题1．心力衰竭最具特征性的血流动力学变化是（）A．肺动脉循环充血B．动脉血压下降C．心输出降低D．毛细血管前阻力增大E．体循环静脉淤血2．下列哪种疾病可引起低输出量性心力衰竭（c）A．甲状腺功能亢进B．严重贫血C．心肌梗死D．脚气病（VitB1缺乏）E．动-静脉瘘3．下列哪项是心肌向心性肥大的特征（b ）A．肌纤维长度增加B．心肌纤维呈并联性增生C．心腔扩大D．室壁增厚不明显E．室腔直径与室壁厚度比值大于正常4．下列哪个肌节长度收缩力最大（）A．1.8μm B．2.0μm C．2.2μm D．2.4μm E．2.6μm5．心力衰竭时心肌收缩性减弱与下列哪项因素无关（）A．ATP 供给不足B．心肌细胞坏死C．肌浆网Ca2+摄取能力下降 D．肌浆网Ca2+释放能力下E．肌钙蛋白活性下降6．下列哪项因素与心室舒张功能障碍无关（）A．甲状腺功能亢进B．心室舒张势能减弱C．心肌顺应性降低D．心室僵硬度加大E．肌浆网Ca2+释放能力下降7．下列哪种疾病可引起左心室后负荷增大（）A．甲状腺功能亢进B．严重贫血C．心肌炎D．心肌梗死E．高血压病8．下列哪种情况可引起右心室前负荷增大（）A．肺动脉高压B．肺动脉栓塞C．室间隔缺损D．心肌炎E．肺动脉瓣狭窄9．下列哪项变化在急性心力衰竭不会发生（）A．心率加快B．肺水肿C．心肌肥大D．血压下降E．皮肤苍白10．下列哪种情况可引起心肌向心性肥大（）A．心肌梗死B．主动脉瓣闭锁不全C．脚气病D．高血压病E．严重贫血11．心功能不全时，通过增加血容量起代偿作用的主要器官是（）A．心B．肝C．脾D．肺E．肾12．下列哪项因素与心肌兴奋-收缩耦联障碍无关（）A．肌钙蛋白活性下降 B．肌球蛋白ATP酶活性下降C．肌浆网Ca2+释放能力下降D．肌浆网Ca2+储存量下降E．Ca2+内流障碍13．心肌缺血引起的心肌收缩性减弱与下列哪个因素无关（）A．ATP生成减少B．心肌细胞死亡C．酸中毒D．肌浆网Ca2+摄取能力降低E．肌钙蛋白与Ca2+结合障碍14．下列哪项不是心脏向心性肥大的特点（）A．肌纤维变粗B．室壁增厚C．心腔无明显扩大D．心肌纤维呈串联性增大E．室腔直径与室壁厚度比值小于正常15．下列哪种疾病引起的心力衰竭不属于低输出量性心力衰竭（）A．冠心病B．心肌炎C．二尖瓣狭窄D．甲状腺功能亢进E．主动脉瓣狭窄16．下列哪项属于心力衰竭时肺循环淤血的表现（）A．肝颈静脉返流征阳性B．夜间阵发性呼吸困难C．下肢水肿D．肝肿大压痛E．颈静脉怒张17．心功能不全时，下列哪项反应已失去代偿意义（）A．心率加快B．心肌肥大C．肌源性扩张D．红细胞增多E．血流重分布18．下列哪项不是心力衰竭时心输出量减少的表现（）A．皮肤苍B．脉压变小C．端坐呼吸D．尿少E．嗜睡19．心力衰竭病人使用静脉扩张剂可以（）A．增强心肌收缩功能B．改善心肌舒张功能C．降低心脏后负荷D．降低心脏前负荷E．控制水肿20．心力衰竭时，下列哪项代偿反应主要由肾脏引起（）A．红细胞增多B．血流重分布C．紧张源性扩张D．肌红蛋白增加E．细胞线粒体数量增多二、问答题1．试述心肌梗死引起心力衰竭的发病机制。
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
病理生理学名词解释资料及问答题 病生名词解释与问答题答案 1.基本病理过程：主要是指多种疾病中可能出现的、共同的、成套的功能、代谢和结构的变化。 2、健康：健康指的是不仅是没有疾病或病痛，而且是一种躯体上、精神上和社会上的完全良好状态。 3、疾病：疾病是在一定条件下受病因损害作用，因机体自稳调节紊乱而发生的异常生命活动过程。 4、病因：能够引起疾病并赋予该疾病特征性的因素称为病因。 5、诱因：能够促进疾病发生发展的因素称为诱因。 6、脑死亡（brain death）： 机体作为一个整体功能永久性停止的标志是全脑功能的永久性消失。目前一般均以枕骨大孔以上全脑死亡的标准 7、低渗性脱水： 又称低容量性低钠血症，其特点是失Na+多于失水，血清Na+浓度<130mmol/L,血浆渗透压<280mmol/L,伴有细胞外液量的减少。 8、高渗性脱水： 又称低容量性高钠血症，其特点是失水多于失Na+,血清Na+浓度>150mmol/L,血浆渗透压>310mmol/L,细胞外液量和细胞外液量均减少。 9、脱水热： 由于从皮肤蒸发的水分减少，使散热受到影响，从而导致体温升高，称之为脱水热。 10、水肿： 过多的液体在组织间隙或体腔内积聚称为水肿。 11、高钾血症： 血清中钾浓度高于5.5mmol/L 12、低钾血症： 血清中钾浓度低于3.5mmol/L 。 13、酸碱平衡紊乱： 病理情况下引起的酸碱超负荷、严重不足或调节机制障碍，导致内环境酸碱稳态破坏而产生PH异常的情况。 14、四型酸碱平衡紊乱： 代谢性酸中毒： 细胞外液H+增加或HCO3- 原发性减少和PH降低为特征的酸碱平衡紊乱类型。 呼吸性酸中毒： CO2排除障碍或吸进过多引起以血浆[H2CO3]原发性增高和PH降低为特征的酸碱平衡紊乱类型。 代谢性酸中毒： 细胞外液碱增多或H+丢失，以血浆[HCO3-]原发性增加和PH升高为特征的酸碱平衡紊乱类型。 呼吸性碱中毒： 肺通气过度，以血浆[H2CO3]原发性减少和PH升高为特征的酸碱平衡紊乱类型。 15、水中毒是指水摄入量超出人体排水量的能力，以致水在体内潴留，引起血液渗透压下降和循环血量增多的病理现象。又称水过、水潴留性低钠或稀释性低钠血症。 16、同一病人有两种或三种单纯型酸碱平衡紊乱同时存在。混合型酸碱平衡紊乱可以有不同的组合形式，通常把两种酸中毒或两种碱中毒合并存在，使pH向同一方向移动的情况称为酸碱一致型或相加性酸碱平衡紊乱。如果是一个酸中毒与一种碱中毒合并存在，使pH向相反的方向移动时，称为酸碱混合型或相消性酸碱平衡紊乱。 17、缺氧（hypoxia):因组织供氧减少或用氧障碍引起细胞代谢、功能和形态结构异常变化的病理过程。 18、发绀（cyanosis）： 当毛细血管血液中脱氧血红蛋白的均匀浓度超过5g/dl时，皮肤和粘膜呈青紫色。 19、四型缺氧： 乏氧性缺氧、血液型缺氧、循环性缺氧、组织性缺氧。 20、肠源性紫绀： 若因进食导致大量血红蛋白氧化而引起的高铁血红蛋白血症。 21、MODS（多器官功能障碍综合症）： 是指在严重创伤、感染、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稳定必须靠临床干预才能维持的综合症。 22、SIRS 及CARS:全身炎症反应(SIRS)： 指因感染或非感染病因作用于机体而引起的失控自我持续放大和自我破坏的全身性炎症反应综合征。 代偿性抗炎反应综合征（CARS):是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过于强烈的内源性抗炎反应。 23、DIC（弥散性血管内出血）： 是一种在致病因子作用下，以凝血系统被激活并引起微血栓形成，同时或继发纤溶亢进， 从而导致出血、休克、器官功能障碍和微血管病性溶血性贫血的一个病理过程。 24、系各种强烈致病因素作用于机体，使循环功能急剧减退，组织器官微循环灌流严重不足，以至重要生命器官机能、代谢严重障碍的全身危重病理过程。 25、心力衰竭： 各种原因引起心脏泵功能障碍，心输出量尽对或相对减少，不能满足组织代谢需要的一种病理过程。 26、充血性心力衰竭： 心力衰竭时，由于心输出量不能与静脉回流相适应，故血液可在静脉系统中淤积。 当心力衰竭呈慢性经过期，往往伴有血容量和组织间液的增多并出现水肿。 27、心肌紧张（肌）源性扩张： 心肌紧张源性扩张： 由于每搏输出量减低，使心室舒张末期容积增加，前负荷增强导致心肌纤维初长度增加，此时心肌收缩力增强，代谢性增加每搏输出量，这种伴有心肌收缩力增强的心腔扩大称为心脏紧张源性扩张。 肌源性扩张： 长期容量负荷过重引起的心力衰竭以及扩张型心肌病，主要引起肌节过度拉长，使心腔明显扩大，这种心肌过度拉长并伴有心肌收缩力减弱的心腔扩大称为肌源性扩张。 28、呼吸衰竭： 由于外呼吸功能严重障碍，使动脉血氧分压低于正常范围，伴或不伴有二氧化碳分压升高的病理过程。 29、限制性通气不足： 吸气时肺泡的扩张受限制所引起的肺泡通气不足。 30、阻塞性通气不足： 由于气道狭窄或阻塞所引起的通气障碍。 31、肺性脑病： 由于呼吸衰竭引起的脑功能障碍，病人可表现为一系列神经精神症状如定向、记忆障碍、精神错乱、头痛、嗜睡、昏迷等。 32、ARDS（急性呼吸窘迫综合症）： 时各种原因引起的肺泡毛细血管膜损伤所致的外呼吸功能严重障碍而发生的以急性呼吸衰竭为特点的临床综合症，主要表现为进行性呼吸困难和低氧血症。 33、肝性脑病： 是指继发于严重肝脏疾病的神经精神综合症。 34、肝肾综合症： 是指肝硬化患者在失代偿期所发生的功能性肾衰及重症肝炎所伴随的急性肾小管坏死。 35、急性肾功能衰竭： 由于GFR急剧减少，或肾小管发生变性、坏死而引起的一种严重的急性病理过程，往往出现少尿、氮质血症、高钾血症、代谢性酸中毒和水中毒等综合症。 36、慢性肾功能衰竭： 任何疾病使肾单位发生进行性破坏，在数月、数年或更长的时间后，残存的肾单位不能充分排除代谢废物和维持内环境恒定、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。 37、肾性高血压： 因肾实质病变引起的高血压称为肾性高血压。 38、尿毒症： 指急性或慢性肾功能衰竭发展到严重阶段，代谢产物和毒物在体内积蓄，水、电解质和酸碱平衡发生紊乱以及某些内分泌功能失调所引起的一系列全身性功能和代谢障碍的综合症。 问答 1.简述脑死亡的诊断标准。 判定脑死亡的根据是①不可逆昏迷和大脑无反应性；②呼吸停止，进行15分钟人工呼吸仍无自主呼吸；③颅神经反射消失；④瞳孔散大或固定；⑤脑电波消失；⑥脑血液循环完全停止（脑血管造影）。 2.哪种类型脱水易造成失液性休克？为什么？ ［答案要点］低容量性低钠血症（低渗性胶水）易引起失液性休克。（1）细胞外液汳透压降低，无口渴感，饮水减少。 （2）细胞外液汳透压降低，ADH反射性分泌减少，尿量无明显减少。 （3）细胞外液向细胞内液转移，细胞外液进一步减少。 3. 水中毒对机体的影响和防治 细胞外液因水过多而被稀释，故血钠浓度降低，渗透压下降。加之肾脏不能将过多的水分及时排出，水分乃向渗透压相对高的细胞内转移而引起细胞水肿，结果是细胞内、外液容量均增多而渗透压都降低。由于细胞内液的容量大于细胞外液的容量，所以潴留的水分大部分积聚在细胞内，因此在轻度水中毒患者，组织间隙中水潴留的程度尚不足以引起明显的凹隐性水肿。急性水中毒时，由于脑神经细胞水肿和颅内压增高，故脑症状出现最早而且突出，可发生各种神经精神症状，如凝视、失语、精神错乱、定向失常、嗜睡、烦躁等并可有视神经乳头水肿，严重者可因发生脑疝而致呼吸心跳骤停，轻度或慢性水中毒患者，发病缓慢，症状常不明显，多被原发病的症状、体征所掩盖，可有嗜睡、头痛、恶心、呕吐、软弱无力及肌肉挛痛等症状。 6.试述水肿时血管内外液体交换失衡的机制？ 机制： 7.简述低钾血症对心肌电生理特性的影响及其机制。 8.低钾血症和高钾血症均可引起肌麻痹，其机制有何不同？请简述之。 低钾血症主要是由于超极化阻滞。 低钾血症时[K+ ] /[K+ ]e 的比值增大，因而肌细胞静息电位负值大，静息电位与阈电位间隔增大，细胞兴奋性于是降低，严得时甚至不能兴奋，亦即细胞处于超极化阻滞状态。 高钾血症由于骨骼肌静息电位过小，因而快钠孔道失活，细胞外于往极化阻滞状态而不能被兴奋。 10.剧烈呕吐易引起何种酸碱平衡紊乱？试分析其发生机制。 剧烈呕吐易导致代谢性碱中毒 机制： ①胃液中H+丢失，使消化道内HCO3-得不到H+中和而吸收进血；②胃液中Cl-丢失，可引起低氯性碱中毒；③胃液中K+丢失，可引起低钾性碱中毒； ④胃液大量丢失，引起有效循环血量减少，继发醛固酮增多。 11.急性肾功能衰竭少尿期可发生什么类型酸碱平衡紊乱？为什么？酸碱平衡指标会有哪些变化？ 答： 发生代谢性酸中毒。 其发生原因： ①GFR（肾小球滤过率）降低，使酸性代谢产物在体内蓄积；②肾小管分泌H+和NH3能力降低，使NaHCO3重吸收减少；③分解代谢增强，固定算产生增多。