Note of Pathophysiology
Chapter1 Introduction for Pathophysiology(P7)
1.Health: State of complete physical, mental, and social well-being and not merely the ab-
sence of disease and infirmity.
2.Disease: Disease is referred as aberrant manifestation of deregulated homeostasis caused by
harmful agents.
3.Brain Death:The criteria of brain death released from WHO are as follows:
i.Cessation of spontaneous respiration;
ii.Irreversible coma;
iii.Absence of cephalic reflexes and dilated pupils;
iv.Absence of any electrical activity of the brain;
v.Absence of brain blood flow.
Chapter2 Cellular disfunction in Disease(P20)
1.细胞增殖(cell proliferation)：是指细胞分裂和再生的过程，细胞通过分裂进行增殖，使
遗传信息传给子代，保留物种的延续性和数量增多。
2.细胞分化(cell differentiation): 是指在细胞增殖时，子代细胞在形态、结构和生理功能上
产生差异的过程，其本质是细胞发生基因差别表达。
3.细胞周期(cell cycle):  或称细胞增殖周期是指增殖细胞从一次分裂结束到下一次分裂结
束所经历的时期和顺序变化，分为四个连续阶段：G1—S—G2—M。
4.细胞凋亡(apoptosis): 由体内外因素触发的细胞内预存的死亡程序，而导致的细胞死亡
过程，称细胞凋亡。是细胞死亡的一种形式。
5.细胞自噬(autophagy or autophagocytosis): 是指细胞利用溶酶体降解自身成分的过程，
被降解的成分包括细胞质以及细胞器。
细胞凋亡过度所导致的疾病：
⑴心血管疾病：①心肌缺血与缺血－再灌注损伤，②心力衰竭
⑵神经细胞退行性疾病:①阿尔茨海默病(Alzheimer’s disease)，②帕金森病、肌萎缩性侧索硬化症脊肌肉萎缩、小脑退行性病、遗传性视网膜退行性变。
⑶病毒感染：艾滋病(acquired immunodeficiency syndrome, AIDS)－－CD4+细胞过度凋亡. 细胞增殖与分化异常与疾病：
Chapter3 Dysfunction of cellular signal transduction in disease(P51) 1.细胞信号转导系统(Cell signaling transduction system)：signal molecules; the coupling re-ceptors /enzyme or an ion channel; intracellular signal transduction pathway.
2.细胞信号转导(Cellular signal transduction)：It is the process of intercellular or intracellular transfer of information through signal transduction pathway.
3.受体病(receptor disease):The receptor can’t mediate the effect of ligand on target cells due to its cha
nging in number, structure and regulation function and leads to disease, this disease is called receptor disease
4.选择题（2/10）
1.弥漫性甲状腺肿（Graves病）的主要信号转导异常是
A 促甲状腺激素分泌减少
B 促甲状腺激素受体下调或减敏
C Gs含量减少
D 刺激性抗体模拟促甲状腺激素（TSH）的作用
E TSH受体阻断性抗体的作用
2.毒素致病作用是
A 促进Gs与受体结合
B 刺激Gs生成
C 使Gs的GTP酶活性增高
D 使Gs的GTP酶活性抑制或丧失
E 抑制Gi与受体结合
3.家族性肾性尿崩症发病的原因是
A 下垂体合成和分泌ADH减少
B 肾小管上皮细胞上的水通道蛋白异常激活
C ADH受体介导的信号转导障碍
D 基因突变使腺苷酸环化酶减少
E 肾小管上皮细胞上的水通道增多
4.重症肌无力的发病环节在
A 乙酰胆碱受体合成数量减少
B 乙酰胆碱受体功能障碍
C 产生了抗N型乙酰胆碱受体的抗体
D 骨骼肌损伤
E 运动终板所释放的乙酰胆碱减少
5.家族性高胆固醇血症属于
A 自身免疫性受体病
B遗传性受体病
C 继发性受体异常病
D G蛋白异常病
E 转录因子异常性疾病    6.重症肌无力属于
A 自身免疫性受体病
B 遗传性受体病
C 继发性受体异常病
D G蛋白异常病
E 转录因子异常性疾病
7.家族性高胆固醇血症的主要病因
A LDL受体基因突变
B LDL存在自身抗体
C 高胆固醇饮食reactive oxygen species名词解释
D高糖饮食
E肝微循环障碍
8.的发病机制是
A 机体毒素受体合成过多
B 毒素具有氯离子通道激活剂作用
C G蛋白合成的增多
D G蛋白的持续激活
E 腺苷酸环化酶合成增多
9.G蛋白激活的关键步骤为
A 配体与G蛋白结合
B GTP与G蛋白的结合
C G蛋白的GTP水解
D G蛋白去磷酸化
E G蛋白与效应器解离
10. 家族性高胆固醇血症的患者LDL受体异常最常见于：
A LDL受体合成障碍
B LDL受体转运障碍
C LDL受体的亲和力下降
D LDL受体内吞缺陷
E LDL受体循环利用异常
Key: 1D 2D 3C 4C 5B 6A 7A 8D 9B 10A
Chapter8 stress(P170)
1.应激反应Stress(or Stress response): “nonspecific response of the body to any
demand made upon it”. Stress is a state of threatened homeostasis. The stress response results in the activation of a complex repertoire of physiological and behavioral adaptive responses, which are relatively non-specific for any stressor that exceeds a threshold.
2.应激原Stressor: Any stimuli, or demands, on body that exceeds a threshold and
cause stress response.
3.应激的神经内分泌机制(Neuroendocrine Responses of stress)
i.sympathetic-adrenal medulla system
ii.hypothalamus-pituitary-adrenal cortex  system, HPA
iii.CNS
iv.Glucocorticoid &Insulin , ADH, etc
4.应激性溃疡(stress ulcer): 指在严重创伤、感染、休克、脑血管意外等应激状态下出
现的胃、十二指肠黏膜的糜烂、浅溃疡、出血。
Stress ulcer is also termed stress gastritis, characterized by superficial and multiple erosions that occur in gastric mucosa, primarily in the fundus of the stomach. The stress ulcer generally develops within 72 hours after a great insult such as severe burning, trauma, hemorrhage, respiratory failure, or
sepsis.
5. 导致应激性溃疡的发生机制(Please describe the mechanism of stress ulcer)大题
⑴Ischemia: Ischemia is thought to be the basic pathogenic mechanism of stress
ulcer.I)Ischemia adversely affect gastric energy metabolism, which is a very important factor in mucosal self-defense against injury.II)Ischemia reduces the capacity of the gastric mucosa to dispose and neutralize acid that enters the tissue.
⑵Counter-diffusion of gastric hydrogen ion to mucosa.
Ischemia and back-diffusion of acid are the two essential pathogenic mechanisms for stress ulcer, but  other intermingled factors may also have important impact on its development. Such as the status of systemic acid-base balance, regeneration of gastric mucosal, level of glucocorticoids, et al.
Chapter 12 Ischemia-reperfusion injury(P248) 1.缺血再灌注损伤的发生机制
i.increase free radicals, ii.calcium overload, utrophils activation,
iv.dysfunction of microcirculation
2.自由基(free radical)：外层电子轨道上含有单个不配对电子的原子、原子团和分子的总
称，也称游离基。
Free radical are a highly reactive group of atoms, molecules or radicals, which carry unpaired electron in outer orbital.
其中，O2·-的生成是其他自由基或活性氧生成的基础，OH·是活性氧中毒性最强的一种。
3.自由基分类(classification of free radical)：氧自由基、脂性自由基、氮自由基。
1)Oxygen free radical,2)Lipid radicals,3)Reactive nitrogen species.
4.自由基的生成机制
i.黄嘌呤氧化途径(increase xanthine oxidase (XO) in VEC)
ii.吞噬细胞呼吸爆发过程产生大量自由基
iii.线粒体电子传递链受损是自由基的主要来源之一
5.活性氧(reactive oxygen species, ROS)单线态氧(˙02)及过氧化氢(H2O2)虽不是自由基，但氧化作用很强，与氧自由基共同称为活性氧。
ROS are composed by oxygen-derived free radicals (OFR) and non-free radical substances, such as superoxide anion radical, hydroxyl radical (OH·), hydrogen peroxide (H2O2) and singlet oxygen (1O2).
6.无复流现象(no-reflow phenomenon)解除缺血原因并没使缺血区得到充分血流灌注的反常现象。
The ischemia region could not be reperfused sufficiently after relieving the occlusion to recover the blood flow.
Basic vasculartonicity is a continual balance between the influences of vasoconstrictors and vasodilatators. Endothelium and the smooth musculature play
a vital part in its control. The conservation of a qualified vasomotricity
improves postischaemic recovery of an organ.
7.黄嘌呤氧化途径(increase xanthine oxidase (XO) in VEC)
Chapter 6 Disorders of water and electrolyte balance(P119) 1. 水钠正常生理
(1)Total body fluid accounts for 60% of body mass in males.intracellular(40%) extra-(15+5%)
(2)细胞内主要阳Na+，阴Cl-/HCO3-；细胞外主要阳K+，主要阴HPO4-。
(3)渗透压、渗量(1mol IN 1L注意阴阳分开算)、正常体液渗透压280-310 mOsm/L
(4)细胞内外水平衡主要靠晶体渗透压维持，血管内外水平衡主要靠胶体渗透压维持。
(5)生理状态下水摄入、排出均2000~2500ml/day
(6)调节机制：1)渴觉[Plasma osmolality↑/Blood volume↓]
2)ADH[Plasma osmolality↑/Blood volume↓/BP↓/Angiotensin II/stress etc.]
3)RAS[Arterial pressure↓/Plasma sodium content↓/Sympathetic nerve↑]
4)ANP[blood volume↑]->利尿排钠舒血管
2.失水表现
①Loss of body weight②Sunken eyes③Depressed fontanel in an infant④Loss of resiliency
of skin⑤Decreased vein filling (collapse) ⑥Hypotension ⑦Elevated body temperature
3.水钠紊乱类型、依据
(1)Hypotonic dehydration(Hypovolemic hyponatremia）
(2)Hypertonic dehydration(hypovolemic hypernatremia)
(3)Isotonic dehydration
(4)Hypotonic fluid volume excess(water intoxication)
(5)Hypertonic fluid volume excess
(6)Isotonic fluid volume(Edema)
依据1)Plasma osmolality<>280-310mmol/L 2)Plasma c(Na+) <>130mmol/L 3)体液量
3.各类型水钠紊乱
(1)Hypotonic dehydration(Hypovolemic hyponatremia）
1)Feature: ①Plasma osmolality<280mmol/L②Plasma Na+ concentration <130mmol/L
③H2O loss < Na+ loss
2)Causes: Excessive sodium losses and replacement with sodium-free water
①Exercise- or heat-induced sweating; ②Burns; ③Gastrointestinal losses
(vomiting, diarrhea); ④Renal losses (diuretic therapy, adrenal Insufficiency)
3)Manifestations
①Shock: No thirst sensation/ Decreased ADH release/ Movement of ECF into cells
②Muscle cramps, weakness, fatigue：hypoosmolality of skeletal muscle cells
③Decreased urine volume④Urine sodium concentration⑤Anorexia, nausea,
vomiting, diarrhea
4)Treatment
①Treatment of the underlying causes ②Administration of saline solution orally
or intravenously

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