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1、Chapter 4： Inflammation,Department of Pathology Peking University Health Science Center Zheng Jie,Skin blister result from burning,Serous effusion accumulated within and underneath the epidermis of skin,Furuncle（疖）,Carbuncle（痈),Outlines of inflammation,General Considerations Definition; Inflammatory
2、 agents; Basic pathological changes of inflammation; Local and systemic manifestations of Inflammation Acute inflammation The process of vascular and cellular events in inflammation, Inflammatory mediators The classification and outcomes of acute inflammationChronic inflammation,Part 1 General Consi
3、derations,Definition,Inflammation is a protective response intended to eliminate the initial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult.,Components of acute and chronic inflammation,Inflammatory agents,Infections (bacterial, viral, parasitic) an
4、d microbial toxins Physical agents (e.g., irradiation, burns) and Trauma (blunt and penetrating) Chemical agents (some environmental chemicals) Ischemic and necrotic tissues Foreign particle (dirt, sutures) Allergic reactions,The basic pathological changes,Alteration (degeneration, necrosis) Exudati
5、on (hallmark, vascular change, leukocyte reaction, inflammatory mediators ) Proliferation (parenchymal and strmal cells),Exudation of plasma proteins,Exudate and transudate,Cause inflammation non-inflammation Gross cloudy clear Gravity 1.018 30g/L 100/mm3 100/mm3 Coagulation + - Mucoprotein + -,Loca
6、l manifestations of Inflammation,rubor (redness) tumor (swelling) calor (heat) dolor (pain),Fever Increased acute-phase proteins Leukocytosis Others: increased pulse and blood pressure; decreased sweating; rigors; anorexia,Systemic manifestations of inflammation,Part 2 Acute inflammation,The process
7、 of acute inflammation,Vascular eventsCellular eventsMolecular events,Vascular Events,Changes in vascular caliber and flow Transient vasoconstriction of arterioles at the site of injury Vasodilation of precapillary arterioles then increases blood flow to the tissue Increased vascular permeability,Th
8、e major local manifestations of acute inflammation: (1) vascular dilation; (2) extravasation of plasma fluid and protein; (3) leukocyte emigration and accumulation in the site of injury,1) Recruitment of leukocytes to sites of infection and injury 2) Recognition of microbes and dead tissues 3) Remov
9、al of the offending agents 4) Release of leukocyte products and leukocyte-mediated tissue injury,Cellular Events,Margination, rolling and adhesion to endothelium Leukocyte migration through endothelium Chemotaxis and activation,1) Recruitment of leukocytes to sites of infection and injury,The multip
10、le process of leukocyte migration through blood vessels.Robbins and Cotran Pathologic Basis of Disease 7th edition,Chemotaxis,After extravasating from the blood, leukocytes migrate toward sites of injury along a chemical gradient in a process called Chemotaxis. Chemotactic Factors including bacteria
11、l products, chemokines, C5a, leukotriene B4,2) Recognition of microbes,Leukocyte receptors and responses,3) Removal of the offending agents,Phagocytosis Engulfment Killing and degradation,Robbins Basic Pathology,A. Phagocytosis: Attachment Engulfment Fusion with lysosomesB. oxygen- dependent bacteri
12、cidal mechanism,4) Release of leukocyte products and leukocyte-mediated tissue injury,Acute inflammation: e.g., acute respiratory distress syndrome; acute transplant rejection; reperfusion injuryChronic inflammation: e.g., arthritis; asthma; chronic lung disease,Inflammatory Mediator,Function of che
13、mical mediators: directing the vascular and cellular events in inflammation Cell-derived or Plasma-derived mediators Act as a complicated network,Cell-derived mediators,Generation of arachidonic acid metabolites and their roles in inflammationRobbins and Cotran Pathologic Basis of Disease 7th editio
14、n,Robbins Basic Pathology,Major effects of IL-1 and TNF,plasma protein-derived mediators,Interrelationships between the four plasma mediators,Role of Mediators in Inflammation,Inflammatory Mediator,Vasodilatation Vascular permeability,EDEMA,VESOACTIVE MEDIATORS Histamine Bradykinin C3a C5a LT PG PAF
15、 NO,TISUE INJURY Trauma Ischemia Neoplasm Infectious agents Foreign particle,PRODUCTION OF INFLAMMATORY MEDIATORS,CHEMOTACTIC FACTORSC5aLTB4 IL-8, TNF,inflammatory cells,ACUTE INFLAMMATIONNeutrophils, Platelets,Mast cell,CHRONIC INFLAMMATION Macrophages, Lymphocytes, Platelets,Classification of infl
16、ammation,Clinical classificationPathological classification,Clinical ClassificationAcute inflammationChronic inflammation,Characteristics of Acute Inflammation,Short duration: days to months Acute injuries induced by inflammatory agents Exudation: fluid, plasma proteins, neutrophils Abscess formation Complete resolution can be reached if the injury is limited or short-lived Severe injury healing by scar formation Spreading : septicemia, pyemia,( metastatic abscess) Progression to chronic inflammation,
