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1、Chapter I. Cellular Adaptation and Cell Injury Responses of cells to different stresses are cellular adaptation, cell injury and cell death. Normal cell Cellular adaptation Cell death Reversible cell injury Atrophy Hypertrophy Hyperplasia Metaplasia Necrosis Apoptosis Degeneration Section I. Cellula
2、r Adaptation Adaptation: cellular response to physiologic or pathological stress showing reversible biochemical, functional, morphologic changes. It is an expression of cell adjustment to the stress and new equilibrium is achieved. The following are examples of such hypertrophy 肥大肥大 hyperplasia 增生增生
3、 atrophy 萎缩萎缩 metaplasia 化生化生( I ). Hypertrophy: Increase in size of the cells or resulting in increase in the size of the organ. It is an adaptation to increase functional demand or stimulation. It implies synthesis of enzymes, mitochondria, endoplasmic reticulums etc. And accompanied by increase i
4、n metabolism. The organ increase in size, weight and volume. 1. physiological hypertrophy e.g. 1). endocrine hypertrophy pregnancy of the uterus 2). muscle hypertrophy in athletes 2. Pathological hypertrophy e.g. hypertensive heart disease (pathological compensatory hypertrophy) 心肌肥大心肌肥大 concentric
5、hypertension( II ). Hyperplasia: Increase number of cells. The organ increase in size, weight and volume. Combined hypertrophy and hyperplasia 1. physiological hyperplasia: e.g. hormonal hyperplasia: pregnancy of the uterus hyperplasia of breast tissue at puberty 2. pathological hyperplasia: e.g. re
6、generation hyperplasia 再生性增生再生性增生 liver cell regeneration Response hyperplasia 反应性增生反应性增生is distinguished from neoplasia.肿瘤性增生肿瘤性增生 ( III ). Atrophy Decrease in size of the cell实质细胞实质细胞 and /or decrease in cell numbers, and therefore in the size of the organ.(the organ decrease in size, weight and v
7、olume) 脂褐素脂褐素 Different: Hypoplasia Aplasia 强调已发育正常再缩小 Essential lesion: parenchymatous cell decrease 实质细胞 mesenchyme is proliferation 增生 间质纤维结缔组织 Physiological atrophy 青春期胸腺，老年女性子宫等 Pathological atrophy According to the cause, pathological atrophy may be classified as: 1. Lack of nutrition: 营养性萎缩 S
8、ystemic atrophy - e.g. 饥饿性萎缩，饥饿性萎缩，cachexia 恶病质 Loss of blood supply - e.g. atherosclerosis, AS Encephlatrophy ( atrophy of the brain) systemic atrophy cachexia Encephlatrophy ( atrophy of the brain) 脑重量减轻，体积缩小脑重量减轻，体积缩小脑回变窄，脑沟变宽脑回变窄，脑沟变宽老年痴呆：老年痴呆： 近事遗忘近事遗忘 性情改变性情改变 2. Disuse atrophy: 废用性萎缩废用性萎缩 It
9、is an adaptation to decrease workload. e.g. bone fracture 骨折骨折 3. Loss of innervation: 去神经性萎缩去神经性萎缩 Loss of innervation of muscle cause muscle atrophy, as is seen in nerve transection. e.g. paraplegia 小儿麻痹症小儿麻痹症 4. Pressure atrophy: 压迫性萎缩压迫性萎缩 This occurrence when tissue are compressed. e.g. nephroh
10、ydrosis hydrocephalus 肾盂积水肾盂积水 5.Loss of endocrine stimulation: 内分泌性萎缩内分泌性萎缩 Atrophy of the target organ靶器官靶器官 of a hormone may occur if endocrine stimulation is inadequate. e.g. the adrenal gland atrophies 肾肾上腺萎缩上腺萎缩 as a consequence of decreased ACTH secretion by the anterior pituitary垂体前叶功能减退垂体前叶
11、功能减退.( IV ). Metaplasia: Transformation of one mature differentiated 分化分化 cell type into another one. Take Note to: (1).(2).(3). 1. Metaplasia in epithelial tissue:( 1 ). Squamous metaplasia e.g. a. respiratory epithelium of the trachea and bronchi in smokers b. chronic cervicitis (erosion of cervix
12、) c. bile ducts in the presence of stones d. transitional bladder epithelium in the presence of stones 支气管鳞状化生总菜单( 2 ). Intestinal metaplasia: e.g. chronic gastritis2. Metaplasia in mesenchymal tissue: e.g. osseous metaplasia bone formation Section II. Cell Injury I. Cause of Cellular Damage ( I ).
13、Hypoxia缺氧缺氧: It is a most important and common cause of cell injury and cell death. Hypoxia may result from: a. Loss of blood supply (Ischemia缺血缺血) Primary arterial disease (atherosclerosis动脉粥样硬化动脉粥样硬化) Intravascular clots (thrombi or emboli血栓或栓塞血栓或栓塞) Circulatory failure 心力衰竭 b. Depletion of oxygen
14、-carring capacity of the blood e.g. Massive hemorrhage 大出血 CO poisoning etc 一氧化碳中毒 c. Action of cellular asphyxiant poisoning of the oxidative enzymes within the cells e.g. Cyanide poisoning氰化物中毒氰化物中毒 which inactivates cytochrome oxidase ( II ). Chemicals and drugs: a. simple chemicals-e.g. Hyperton
15、ic glucose, salt, may cause cell injury b. Chemical posisons-e.g. Cyanide氰化物氰化物, Hg salts汞盐汞盐 ( III ). Physical agent: a. trauma b. extremes of heat or cold are the common physical causes that injury the cell and tissue. c. Nuclear explosion and large doses of therapentic radiation. Electromagnetic
16、waves, X-Ray. ( IV ). Biological Agents Include the virus, rickettside , bacteria, fungi and higher forms of parasites Bacteria: liberating exetoxin release of endotoxin from the cell walls when the bacteria are killed Virus: alters cell antigen causing mutation intracellular growth Parasites: elabo
17、rating enzyme, such as proteolytic enzyme from amoba ( V ). Immunological Reactions ( VI ). Genetic Derangements ( VII ). Nutritional Imbalances ( VIII ). Other: Endocrine Factor, Aging Psychosomatic disease 心身疾病心身疾病 Iatrogenic disease 医源性疾病 II. Mechanism of Cell Injury 1. to impairment of ATP gener
18、ation 2. damage to mitochondria 3. damage to membrane permeability 4. to increased Ca+ into intracellular 5 free radical Free radical is very reactive and unstable. Reacting with chemical in the cell membrane and nucleic. IV. Morphological Change of the Cell Injury ( I ). Reversible cell injury (Deg
19、eneration ) 细胞细胞 细胞间质细胞间质 出现异常物质出现异常物质 正常物质积聚过多正常物质积聚过多 1. Cellular swelling (hydropic degeneration) Cause: hypoxia , bacteria toxin, intoxication etc. Mechanism: Damage of plasma membrance, hence increase permeability with loss of potassium, influx of sodium water, and calcium. Damage of mitochondr
20、ia decrease ATP and consequently failure of the “pump” Morphology: Gross: Increase in size and weight of the affected organ, and loss of normal glistening transluscency boiled meat appearance. LM: Swollen of the affected cell, with fine granule and vacuoles filling the cytoplasm There are large vacu
21、oles in the cytoplasm sometime appear ballooning change 气球样变 EM: Swollen mitochondria and endoplasmic reticulum. Nucleus not affected. 2. Fatty Degeneration (fatty change) Absolute increase in intracellular lipid. Accumulation of neutral fat 中性脂肪（甘油三酯中性脂肪（甘油三酯 ）vacuoles in the parenchymatous cells.
22、好发器官：好发器官： Liver cell, Heart muscle cells, Renal tubule epitheliaMechanism 发病机理发病机理：血液中被吸收血液中被吸收脂肪酸氧化脂肪酸氧化 （降解）（降解） 入入出出 脂肪酸脂肪酸肝细胞肝细胞脂蛋白合成脂蛋白合成（进入血液（进入血液/进入脂库贮存）进入脂库贮存）碳水化合物合成碳水化合物合成细胞结构脂肪细胞结构脂肪 Morphology: LM: Empty vacuoles in the cytoplasm large vacuole pushes nucleus against the cell membrance.
23、In the frozen section fat can be demonstrated by fat soluble dyes (suden III-orange ) 脂肪特染 (苏丹黑)总菜单( 1 ). Fatty change of liver Gross: enlarged, rounded edge, yellowish and greasy Hepative steatosis (fatty liver脂肪肝脂肪肝) LM: ( 2 ). Fatty change of heart focal change: severe anemia full change: poisoni
24、ng 虎斑心虎斑心 Fatty infiltration心肌脂肪浸润（脂肪心）：心肌脂肪浸润（脂肪心）： Should not be confused with fatty degeneration. It is an accumulation of adipose tissue in the interstitium usually cause pressure atrophy of the adjacent parenchyma. 3. Amyloid change 淀粉样变性淀粉样变性 Amyloidosis Focal change: - Alzheimer disease 4. Hy
25、aline change (hyaline degeneration) 细细胞胞内内或或间间质质中中出出现现HE染染色色均均质质性性伊伊红红色色半半透明状的蛋白质蓄集称为玻璃样变性或透明变性透明状的蛋白质蓄集称为玻璃样变性或透明变性 ( 1). Hyaline degeneration of connective tissue: One of the most common types of connective tissue alteration with deposition of mucopolysaccharide or protein, swelling of collagen fi
26、bers. The affected tissue become stiff, resilient , translucent grossly, and stained by acid dyes, such as eosin. ( 2 ). Hyaline degeneration of blood vessels: Infiltration of plasma protein in the arterioles. e.g. a. primary hypertension 原发性高血压原发性高血压 b. diabetes mellitus 糖尿病糖尿病 ( 3 ). Intracellular
27、 Hyaline Droplets:a. Protein droplets： lipoid nephrosis b. Immunoglobulin： Ig within the cistenae of RER forming hyaline droplets (russells body) of plasma cell. c. Mallory body (alcoholic hyaline body)： alcoholic liver disease 5. Mucoid change 粘液样变性粘液样变性 (mucoid degeneration) Mucoid formed by mesen
28、chymal tissue. It is mucopolysaccharide. alcian blue normally it should be blue mucin: secreted by mucous glands is also glyprotein. 6. Pathologic pigmentation 病理性色素沉着病理性色素沉着 1 ).Hemosiderin含铁血黄素：含铁血黄素：Formed when here is local excessive hemorrage, large amount of RBC is destroyed. It is a golden ye
29、llow brownish granules. They are found in the phygocytes. Heart failure cell 心力衰竭细胞心力衰竭细胞 Prussian blue histochemical reaction yields positive result. ( 2 ). Lipofuscin 脂褐素脂褐素 Under LM it appears as yellow brown fine cytoplasmic insoluble granules. They are found in heart muscle and liver cell of ag
30、ing individual. EM: autophagic vacuoles residual body 7. Pathologic calcification Dystrophic calcification 营养不良性钙化营养不良性钙化: Refers to deposits on dead tissue. Calcium metabolism is normal. Metastatic calcification 转移性钙化转移性钙化: Encountered in a normal tissue. Deranged calcium metabolism, leading to hyp
31、ercalcemia. Usually occur in kidney, lung, gastric mucosa, where acid salts are excreted. ( II ). Cell Death （III）1. Necrosis 坏死坏死 ： Tissue, cell death in living organisms. 酶解性变化，活体，局部 Irreversible cell injury Autolysis 自溶自溶- a process of dissolution of cell by self-digestion through activition and
32、release of lysosomal enzymes Heterolysis 异溶异溶- Digestion dead cell by lysosomal enzymes released by the immigrated leukcytes. ( 1 ). Essential change of the necrosis Biochemical change is early than morphological change. e.g. myocardial infarction, MI 2h, SGOT LDH 4-12h, morphological change Hallmar
33、ks of cell death nuclear change 1 ). nuclear change The nuclear change appears in one of the three forms: a. Pyknosis - nuclear shrinkage of condensation b. Karyorrhexis - fragmentation or break up of chromatin. c. Karyolysis - lysis or fading away of chromatin, results in absence of nucleus. 2 ).pl
34、asm and plasmalemma change intracellular acidity membranolysis 膜溶解膜溶解 inflammatory response 炎症反应炎症反应. 3 ).mesenchyma change间质变化：间质变化： devitalized tissue 失活组织 devitalized tissue (infarct of intestin) ( 2 ). Type of necrosis 1 ). Coagulative necrosis 凝固性坏死凝固性坏死 denaturation of protein proteolysis of t
35、he cells is blocked. sudden complete blockage of blood supply. It occure characteristically in the myocardium, lung, kidney, spleen etc. Morphological characteristics ( Gross and LM) 脾凝固性坏死总菜单大体特点：蛋白凝固、干燥、边界清楚大体特点：蛋白凝固、干燥、边界清楚 coagulative necrosis镜下特点：组织轮廓保留一段时间镜下特点：组织轮廓保留一段时间 2 ). Liquefactive necr
36、osis 液化性坏死液化性坏死 The damaged cells are lysed into fluid and semifluid material Both autolysis and heterolysis prevail e.g. a. encephalomalacia b. lysis necrosis c. abscess d. amoebiasis e. fat necrosis 3 ). Special type of necrosis a. Caseous necrosis 干酪样坏死干酪样坏死 a special form of coagulative necrosis
37、. Gross: It is yellowish cheese in appearance LM: The necrosis tissue appears as an eosinophilic amorphous granular debris. e.g. Tuberculous infection b. Gangrene坏疽坏疽: 大块组织、继发改变大块组织、继发改变 Massive necrosis of tissue with superadded putrefection caused by the action of saprophytic organisms Black color
38、 is due to the pressence of FeS2 produced by the break down of hemoglobin. Dry Gangrene : 干性坏疽干性坏疽Wet Gangrene (moist gangrene) 湿性坏疽湿性坏疽Gas Gangrene : 气性坏疽气性坏疽干性坏疽干性坏疽湿性坏疽湿性坏疽好发部位好发部位四肢末端四肢末端四肢末端、阑尾、胆四肢末端、阑尾、胆囊、肠、肺和子宫囊、肠、肺和子宫发病条件发病条件动脉阻塞，静动脉阻塞，静脉回流通畅脉回流通畅动静脉同时阻塞动静脉同时阻塞病变特点病变特点坏坏死死干干燥燥，与与周周围围健健康康组组织织
39、之之间间分分界界线线明明显显。坏死组织肿胀，坏死组织肿胀，湿润湿润。与与健健康康组组织织分分界界线线不不明显。明显。对机体影对机体影响响中毒症状轻中毒症状轻中毒症状重中毒症状重临床上常见的干性坏疽可见于临床上常见的干性坏疽可见于：动脉粥样硬化动脉粥样硬化血栓闭塞性脉管炎血栓闭塞性脉管炎冻伤等疾患冻伤等疾患临床上常见的湿性坏疽有临床上常见的湿性坏疽有：坏疽性阑尾炎坏疽性阑尾炎肠坏疽肠坏疽肺坏疽肺坏疽产后坏疽性子宫内膜炎产后坏疽性子宫内膜炎临床上气性坏疽主要见于：临床上气性坏疽主要见于：严严重重的的深深达达肌肌肉肉的的开开放放性性创创伤伤，同同时时伴伴有有产产气气炎炎膜膜杆杆菌菌、恶恶性性水水肿肿
40、杆杆菌菌及及腐腐败败弧弧菌菌等厌气菌感染。等厌气菌感染。坏坏死死组组织织内内含含气气泡泡呈呈蜂蜂窝窝状状，按按之之有有稔稔发发音，厌气菌分解坏死组织，产生大量气体。音，厌气菌分解坏死组织，产生大量气体。为湿性坏疽的一种特殊类型为湿性坏疽的一种特殊类型c. Fat necrosis enzymelysis fat necrosis: e.g. acute pancreatitis 急性胰腺炎急性胰腺炎 trauma fat necrosis: e.g. breast trauma d. Fibrinoid necrosis 纤维素样坏死：纤维素样坏死： Occurrence-part: Conn
41、ective tissue Vessel wall 胶原病胶原病 坏死性血管炎坏死性血管炎 LM: Intensely eosinophilic stain Collagen disrupted +IC True fibrin is present in vessel wall 补体激活补体激活 中性白细胞中性白细胞 ( 3 ). Sequel of necrosis 1 ). Lysis and absorption 2 ). Removed : Removed by inflammatory response by phagocytosis of leukocytes. 3 ). Orga
42、nization and encapsulation : One of the fundamental processes in pathology, can be defined as the replacement of necrosis (or inflammatory exudate , thrombus, blood clot ) by granulation tissue. 4 ).Calcification 2. Apoptosis Cell suicide programmed cell death (PCD) The feuture of morphological chan
43、ge is forming apoptotic bodies. e.g. Councilman bodies Tangible bodies Comparison of cell death by necrosis and apoptosis Tab1-1 comparison of cell death by necrosis and apoptosis Feature Necrosis Apoptosis Induction: Invariably due to pathological injury May be induced by physiological or pathologi
44、cal stimuli Histological change: Extent Cytoplasm Organelle Cell membrane Cell groupsSwelling and lysisSwelling-brokenLost. The cell lysis Single cellShrinkageDenseMaintainedForming apoptotic bodies Chapter II Repair and Healing Repair Replacement of dead cells by viable cellsHealing An aspect of re
45、pair Closure of some gap as in a wound or an ulcer. Regeneration Replacement of the cell loss by production of more cells of the same kind. Complete regeneration 完全再生完全再生 replacement of the cell loss by the regeneration of same type of cells Incomplete regeneration (fibrous repair) 纤维性修复纤维性修复 replac
46、ement of the cell loss by connective tissue, forming scar. I. The Cell Cycle and Regenerative Capacity of Somatic Cells G1 phase Interphase S phaseCell cycle G2 phase Mitotic phase (Division) Regenerative capacity of somatic cells 1. Labile cell 不稳定细胞，持续分裂细胞不稳定细胞，持续分裂细胞 continuously dividing cell Co
47、ntinue to multiply throughout life to replace those shed or destroyed during physiological process. It include epidermis, alimentory, respiratory and urinary tract epithelum, uterine endometrim, hemopoietic bone marrow, lymphoid. Section I Regeneration Physiological regeneration Pathological regener
48、ation 2. Stable cells 稳定细胞稳定细胞 quiescent cell 静止细胞静止细胞 Normally cease multiplication when growth cease but retain mitotic ability during adult life, so that some regeneration of damage tissue may occur. It include liver, pancrease, renal tubules epithelium, thyroid and adrenal cortex 3. Permanent ce
49、ll 永久细胞永久细胞 nondividing cell 非分裂细胞非分裂细胞 Loss their mitotic ability Comprise neurons and skeletal and cardiac muscle cell II. Regeneration course of various kind of tissue ( I ). Epithelium regeneration 1. Cover epithelium regeneration 2. Glandular epithelium Hepatocyte regeneration: ( II ). Fibrous
50、tissue regenerationfibroblast collagenation fibrocyte collagen fibers ( III ). Cartilage regeneration Cartilage regenerative capacity is weak ( IV ). Angiogensis 1. Capillary regeneration 2. Large blood vessel regeneration ( V ).Muscular regeneration The capacity of muscular regeneration is weak. St
51、riated muscle: According to the damage of sarcolemma Smooth muscle: Cardiac muscle: ( VI ). Nerve tissue regeneration (neuranagenesis) Section III Fibrous repair I. Morphylogy and function of granulation issue( II ). Compose and morphylogy of granulation tissue Granulation tissue Composed of newly f
52、ormed capillary loops , fibroblast and inflammatory cells. Myofibroblast ( II ). Function and Sequel of granulation tissueFunction: a. Anti-infection and protection of traumatism b. Fill the traumatism c. Organization: to replace useless material Sequel: Devascularization-fibroplasia: atrophy and ob
53、literation of blood vessels Forming pale and avascular scar tissue II. Scar benefit harmful: a.Contraction b. Synechia c. Excessive proliferation Keloid formation excessive formation of collagenous Section IV Wound Healing I. Healing of a skin wound The process of healing of a skin wound depends on
54、the size of the defect. ( I ). The course of wound healing 1. Change of early period: removal of inflammatory 2. Wound contraction: 2-3 days The contraction force is generated by myofibroblasts of granulation tissue. 3. Proliferation of granulation tissue and formation of scar 3th, 5-6 days : collag
55、enization 1 month : complete formation of scar 4. Epidermis regeneration ( II ). Types of wound healing comparison of two types of wound healing Characteristic Healing by first intention Healing by second intention defect size small large suture usually, yes no infection no yes amount of necrotic ti
56、ssuesmalllargeamount of granulation tissue small largescar size very small largerate of healing rapid slow complication rarely keloid II. Healing of bone fracture Traumatic bone fracture Pathological bone fracture Healing of bone fracture consists of 4 stepshematoma fibrous callus osseous callus cal
57、lusforming forming forming reconstruct III. Factors influence wound healing( I ). Systemic factors 1Aging 2. Nutrition: nutritional imbalance protein 甲硫氨酸、蛋氨酸等含硫甲硫氨酸、蛋氨酸等含硫 氨基酸氨基酸 deficiency, Vitamin C, or Zn deficiency ( II ). Local factors 1. infection and foreign body 2. local vascular supply 3. innervation 4. radiation ( III ). Factors influence bone fracture: 1.reduction 2.fixed 3. take exercise
