第二章 损伤的修复

第二章损伤的修复一、名词解释1．修复(repair)2．再生(regeneration)3．不稳定细胞(labile cell)4. 稳定细胞（stable cells)5．永久性细胞(permanent cell)6．接触抑制(contact inhibition)7*．创伤性神经瘤(traumatic neuroma)8*. 生长因子(cell growth factors)9. 肉芽组织(granulation tissue)10.瘢痕组织(scar tissue)11．瘢痕疙瘩(keloid)12．创伤愈合(wound healing)13*．痂下愈合(healing under scab)14*.细胞外基质(extracellular matrix, ECM) 二、填空１．组织损伤的修复包括①----、②----2种不同过程。

２．生理性再生可发生在①----、②----、③----、④----等器官、组织。

３．按再生能力的强弱，可将人体组织细胞分为①----、②----、③----3类。

４．稳定细胞在生理情况下处于细胞增殖周期中的①----，但受到组织损伤的刺激时，则进入②----，表现出较强的再生能力,例如③----细胞。

５．胃肠黏膜上皮缺损后通过①----修复，纤维组织的再生是通过②----修复，毛细血管以③----方式再生，心肌损伤破坏后一般发生④----修复，皮肤附属器损伤后发生⑤----修复。

６．短距离调控细胞再生的重要因素有以下3方面：①----，②----，③----。

７．请列举4种细胞生长因子：①----，②----，③----，④----；抑制上皮增殖，促进间质细胞增殖的生长因子为⑤----。

#８ *.胶原纤维的生成过程是①----在生长因子刺激下将②----分泌到细胞外，被③----酶切去两端球形结构，形成④----，后者相互错开1/4平行排列交联成⑤----，再进一步聚合成较宽的⑥----。

#9．根据不同的化学成分将胶原分为①----种，间质中的胶原纤维由②----和③----组成，网状纤维的主要成分是④----。

10.伤口创伤愈合的基本过程包括①----、②----、③----、④----。

11．根据损伤程度及有无感染，创伤愈合可分为以下2种类型：①----、②----。

１2．①----②----③----决定修复的方式、愈合的时间及瘢痕的大小，因此对损伤的治疗原则应是④----、⑤----和⑥----。

三、选择题(一)Ａ型题（１～１０）１．下列各种细胞再生能力最强的是：A.表皮细胞B.平滑肌细胞C.肾小管上皮细胞D.血管内皮细胞E.软骨母细胞２．下列具较强再生能力又有很强分化能力的细胞是： A.表皮细胞B.呼吸道黏膜被覆细胞C.子宫内膜上皮细胞D.原始间叶细胞E.内分泌腺上皮细胞３．下列能促进纤维母细胞增生的是：A.层粘连蛋白B.肿瘤坏死因子C.干扰素-αD.肝素E.前列腺素E 2４．肉芽组织转化为瘢痕组织的过程中不会发生：A.网状纤维及胶原纤维增多B.炎症细胞消失C.玻璃样变D.毛细血管闭合、退化E.纤维母细胞减少５．关于创伤一期愈合正确的是：A.无感染故无炎症，仅有表皮再生，无肉芽组织生长B.无感染，有轻度炎症，表皮再生先于肉芽组织生长C.无感染故无炎症，表皮再生先于肉芽组织生长D.无感染，有轻度炎症，肉芽组织生长填平伤口后表皮再生覆盖E.无感染故无炎症，肉芽组织生长填平伤口后表皮再生覆盖６．关于再生下列可能发生的是：A.一侧肾脏摘除后，另一侧肾脏体积增大B.胃肠道黏膜缺损后由表层上皮增生修补C.神经细胞通过脱髓鞘后再生D.分化低的组织再生能力强E.横纹肌损伤均不能再生７．一期愈合的手术切口，一般在术后多长时间可拆线?A.第３天B.第５～６天C.２周D.３周E.以上都不是８ *．下列数据正确的是：A.神经纤维再生时近端轴突每天可伸长10 mmB.神经纤维断离两端超过3.5 cm时，才形成创伤性神经瘤C.伤口直径达10 cm时，表皮难以再生，而必需植皮D.肉芽组织形成时，毛细血管每日延长0.1～0.6 mmE.以上都不是９ *．维生素Ｃ在创伤愈合中的作用是：A.促进含硫氨基酸吸收、合成B.促进前胶原分子形成C.促进胶原纤维的交联D.促进胶原原蛋白的合成E.抑制胶原纤维的形成１０．影响伤口愈合的局部因素不包括： A.严重感染B.电离辐射C.含硫氨基酸缺乏D.局部血液循环不良E.手术缝线(二)Ｂ型题（１１～２０）A.肿瘤坏死因子(TNF)B.细胞间缝隙连接C.层粘连蛋白D.细胞的基因活化、表达E.前列腺素Ｅ ２１１．接触抑制１２．血管再生１３．细胞周期１４．上皮细胞增殖１５．抑制平滑肌增殖A.肥大B.增生C.化生D.再生E.机化１６．月经期后的子宫内膜１７．胆囊结石，胆囊黏膜内出现鳞状上皮 １８．妊娠期的子宫１９．脾贫血性梗死的修复２０．慢性肝炎时肝细胞分裂增殖(三)Ｃ型题(２１～２９)A.完全再生B.瘢痕修复C.两者均有D.两者均无２１．胃溃疡愈合２２．病毒性肝炎点状坏死２３．开放性骨折愈合２４．脑脓肿２５．脾脏造血细胞增生A.一期愈合B.二期愈合C.两者均有D.两者均无２６．炎症反应２７．不形成瘢痕２８．表皮再生先于肉芽组织形成 ２９．发生气性坏疽的开放性创伤(四)Ｘ型题（３０～４０）３０．下列属于永久性细胞的是：A.神经细胞B.神经胶质细胞C.骨骼肌细胞D.心肌细胞E.平滑肌细胞３１ *．下列各项可促进上皮细胞增殖的是：A.基质中的层粘连蛋白(LN)B.基质中的纤维粘连蛋白(FN)C.血小板源性生长因子(PDGF)D.转化生长因子-α (TGF-α)E.转化生长因子-β (TGF-β)３２．肉芽组织镜下可见：A.内皮细胞B.神经细胞C.炎性细胞D.纤维母细胞E.肌纤维母细胞３３．关于肉芽组织的描述，下列正确的是：A.由新生的毛细血管和纤维母细胞组成B.均有炎症细胞浸润，因此有抗感染功能C.是纤维性修复的必经之路D.毛细血管内皮细胞可分泌多种生长因子E.毛细血管内皮细胞具有吞噬能力３４．下列可发生完全再生的是：A.所有的生理性再生B.骨折的修复C.断离的大血管经手术吻合后D.皮肤附属器完全被破坏后E.断裂的肌腱经手术缝合后３５．冠心病心肌梗死后：A.及时治疗心肌细胞可完全再生B.局部发生凝固性坏死C.发生纤维性修复D.形成室壁瘤E.可发生心脏破裂３６．与伤口收缩呈正相关的因素有：A.胶原纤维B.肌纤维母细胞C.糖皮质激素D.去甲肾上腺素E.植皮３７．下列关于瘢痕形成的叙述正确的是：A．瘢痕中的胶原纤维最终与皮肤表面平行B．与腹壁疝有关C．脑液化性坏死后通过纤维瘢痕修复D．瘢痕的抗拉力强度可与正常皮肤相同E．瘢痕的抗拉力强度主要由胶原纤维的量及其排列状态决定３８．肉芽组织可出现在：A．手术切口修复过程B．血栓机化的过程C．溃疡底部和边缘D．胸膜炎胸腔积液E．脓肿壁形成过程３９．瘢痕修复可引起哪些不良后果：A．胸膜腔粘连B．肠腔狭窄C．心瓣膜变形D．关节僵直，运动障碍E．瘢痕疙瘩４０．关于伤口愈合下列正确的是：A．下肢静脉曲张时伤口愈合迟缓B．神经的损伤与否对愈合不产生影响C．感染的伤口可以缝合以缩小创面，促进愈合D．伤口感染时，局部张力增加，可导致感染扩散而加重损伤E．清创缝合术可以使有较多坏死组织的伤口达到一期愈合四、英汉对照阅读1.Regeneration and wound healing⑴RegenerationCells are divided into three groups on the basis of their capacity to regenerate:①Labile cells (surface epithelia,hematopoietic cells) continue to proliferate throughout life, replacing cells that are continuously being destroyed.With injury and loss of cells,complete regeneration is possible from remainingcells.②Stabile cells (liver,connective tissue) normally have a low level of replication but can undergo rapid division in response to physiologic and pathologic stimuli,thus reconstituting the tissue of origin。

③Permanent cells (nerve cell, skeletal and cardiac muscle cells)essentially do not regenerate.Labile cells follow the cell cycle from one mitosis to the next.Permanent cells have left the cell cycle and are destined to senesce and die. Stabile cells are at G 0 but are stim ulated into G 1 by an appropriate stimulus. Arrest at G 2 before entering mitosis results in the appearance of polyploid cells-characteristic of cells that have undergone hypertrophy but cannot undergo division.⑵Wound HealingHealing of a clean surgical approximated incision ( first intention)involves an orchestrated sequence of events,as follows:0 hours. The incision is filled with clot.3 to 24 hours. Neutrophils from the margins infiltrate the clot. Mitoses begin to appear in epithelial basal cells; epithelial closure takes place by 24 to 48 hours.Day 3.Neutrophils are replaced by macrophages. Granulation tissue begins to appear.Day 5. The incision space is filled with granulation tissue,neovascularization is maximal,collagen fibrils begin to appear, and epithelial proliferationis now maximal.Week 2. There is proliferation of fibroblasts and continued collagen accumulation. Inflammation and newly formed vessels have largely disappeared.Month 2. Scar now consists of connective tissue devoid of inflammation covered by intact epidermis.Healing with second intention occurs when there is more extensive loss of tissue,such as infarction, ulceration, abscess formation, and large wounds.Abundant granulation tissue grows in from the margins to fill the defect,but at the same time the wound contracts; i. e. , the defect is markedly reduced from its original size. Myofibroblasts contribute to wound contraction.2. Collagenization and Wound StrengthCollagen fibers account in large part for wound strength.Adult skin collagen is mostly type I,but collagen deposited early in granulation tissue is type III,which is then replaced by adult type I collagen Wound strength at the end of the first week is approximately 10%;it is largely dependent on surgical suturing andtissue-tissue adhesion.Strength reaches 70 to 80%by the third month and then plateaus.Wound collagen is in a constant state of turn over.Collagenases that are present in a variety of cell types, including fibroblasts,macrophages and neutrophils,cleave collagen into fragments that are susceptible to digestion by other proteases.Collagen degradation may aid in the debridement of injured sites and in the remodeling of connective tissue necessary for the healing of a defect.However,collagenase may contribute to continuing tissue damage in some chronic inflammatory disorders such as rheumatoid arthritis.Other extracellular matrix components include elastic fibers, glycosaminoglycans, laminin, and fibronectin. Fibroblasts and myofibroblasts secrete collagens,elastins,and proteoglycans in healing wounds,and such secretion is modulated by growth factors derived from macrophages,platelets,and lymphocytes.For example,IL-1 and TNF stimulate both collagen and collagenase formation by fibroblaste,and TGF-β also stimulates collagen synthesis. Laminin and fibronectin are large,multifunctional glycoproteins involved in cell attachment, migration, and differentiation.(以上短文摘自Stanley L.Robbins等编Pathdogic Basis of Disease)[KG*2]3.Fibrosis (Fibroplasia)Fibrosis or fibroplasia occurs on the granulation tissue framework of new vessels and loose ECM that develop early at the repair site. The process of fibrosis occurs in two steps: (1) emigration and proliferation of fibroblasts in the site of injury , and (2) deposition of ECM by these cells. The recruitment and stimulation of fibroblasts is driven by the various growth factors . The sources of these growth factors include activated endothelium, but perhaps more importantly , they also include a variety of inflammatory cells. Macrophages, for example , areimportant cellular constituents of granulation tissue, responsible for clearing extracellular debris, fibrin, and other foreign matter at the site of injury; they also elaborate PDGF,b-FGF, and TGF-βand therefore promote fibroblast migration and proliferation. If the appropriate chemotactic stimuli are present, lymphocytes may also be present, and mast cells are increased in number ; each of these can contribute directly or indirectly to fibroblast proliferation and activation.As healing progresses, the number of proliferating fibroblasts and new vessels decreases ; however , the fibroblasts progressively assume a more synthetic phenotype, and hence there is increased deposition of ECM. Collagen synthesis , in particular, is critical to the development of strength in a healing wound site. As described below, collagen synthesis by fibroblasts begins early on wound healing (days 3 to 5) and continues for several weeks , depending on the size of the wound. Many of the same growth factors that regulate fibroblast proliferation also participate in stimulating ECM synthesis. Collagen synthesis,for example , is induced by a number of the molecules, including growth factors (PDGF,b-FGF, and TGF-β) and cytokines (IL-1 and TNF ) secreted by leukocytes and fibroblasts . Net collagen accumulation, however, depends not only on increased synthesis but also on diminished collagen degradation . Ultimately, the granulation tissue scaffolding evolves into a scar composed of largely inactive, spindle-shaped fibroblasts , dense collagen, fragments of elastic tissue , and other ECM components.(以上短文选自Vinay Kamak等编，Basic Pathology, 第6版)五、问答题１．简述修复的两种不同过程。