1、Department of PathologyDepartment of PathologyPeking UniversityPeking UniversityHealth Science Center Health Science Center Zheng JieZheng JieSkin blister result from burningSerous effusion accumulated within and underneath the epidermis of skinFuruncle（疖）Carbuncle（痈) protectiveComponents of acute a
2、nd chronic inflammationlInfections (bacterial, viral, parasitic) and microbial toxinslPhysical agents (e.g., irradiation, burns) and Trauma (blunt and penetrating) lChemical agents (some environmental chemicals) lIschemic and necrotic tissues lForeign particle (dirt, sutures) lAllergic reactionsmm3m
3、m3 lrubor (redness)ltumor (swelling)lcalor (heat)ldolor (pain)lFeverlIncreased acute-phase proteinslLeukocytosislOthers: increased pulse and blood pressure; decreased sweating; rigors; anorexia The major local manifestations of acute inflammation: (1) vascular dilation; (2) extravasation of plasma f
4、luid and protein; (3) leukocyte emigration and accumulation in the site of injury The multiple process of leukocyte migration through blood vessels. Robbins and Cotran Pathologic Basis of Disease 7th editionLeukocyte receptors and responses3) Removal of the offending agentslPhagocytosislEngulfmentlK
5、illing and degradationRobbins Basic PathologyA. Phagocytosis:lAttachmentlEngulfmentlFusion with lysosomesB. oxygen-dependent bactericidalmechanismlAcute inflammation: e.g., acute respiratory distress syndrome; acute transplant rejection; reperfusion injurylChronic inflammation: e.g., arthritis; asth
6、ma; chronic lung disease lFunction of chemical mediators: directing the vascular and cellular events in inflammationMediators Sources ActionsHistamineMast cells, basophils, plateletsVasodilation, increased vascular permeability, endothelial activationSerotoninPlateletsVasodilation, increased vascula
7、r permeabilityProstaglandinsMast cells, leukocytesVasodilation, pain, feverLeukotrienesMast cells, leukocytesIncreased vascular permeability, chemotaxis, leukocyte adhesion and activationPlatelet-activating factorLeukocytes, mast cellsVasodilation, increased vascular permeability, leukocyte adhesion
8、, chemotaxis, degranulation, oxidative burstReactive oxygen speciesLeukocytesKilling of microbes, tissue damageNitric oxideEndothelium, macrophagesVascular smooth muscle relaxation, killing of microbesCytokines (TNF, IL-1)Macrophages, endothelial cells, mast cellsLocal endothelial activation (expres
9、sion of adhesion molecules), fever/pain/anorexia/hypotension, decreased vascular resistance (shock)ChemokinesLeukocytes, activated macrophagesChemotaxis, leukocyte activationCell-derived mediatorsGeneration of arachidonic acid metabolites and their roles in inflammation Robbins and Cotran Pathologic
10、 Basis of Disease 7th editionRobbins Basic PathologyMajor effectsof IL-1 and TNFMediators Sources ActionsComplement products (C5a, C3a, C4a)Plasma (produced in liver)Leukocyte chemotaxis and activation, vasodilation (mast cell stimulation)KininsPlasma (produced in liver)Increased vascular permeabili
11、ty, smooth muscle contraction, vasodilation, painProteases activated during coagulationPlasma (produced in liver)Endothelial activation, leukocyte recruitmentplasma protein-derived mediators Interrelationships between the four plasma mediators Role in InflammationMediatorsVasodilationProstaglandins,
12、 Nitric oxide, HistamineIncreased vascular permeabilityHistamine and serotonin, C3a and C5a,BradykininLeukotrienes C4, D4, E4, PAF, Substance PChemotaxis, leukocyte recruitment and activationTNF, IL-1, Chemokines, C3a, C5a, Leukotriene B4FeverIL-1, TNF, ProstaglandinsPainProstaglandins, BradykininTi
13、ssue damageLysosomal enzymes of leukocytes, Reactive oxygen speciesNitric oxide Role of Mediators in Inflammation HistamineBradykininC3a C5aLT PGPAFNOTraumaIschemiaNeoplasmInfectious agentsForeign particle C5a LTB4IL-8, TNFNeutrophils, Platelets,Mast cell Macrophages,Lymphocytes, Platelets Classific
14、ation of inflammationlClinical classificationlPathological classification Characteristics of Acute InflammationlShort duration: days to monthslAcute injuries induced by inflammatory agentslExudation: fluid, plasma proteins, neutrophilslAbscess formation lComplete resolution can be reached if the inj
15、ury is limited or short-livedlSevere injury healing by scar formationlSpreading : septicemia, pyemia,( metastatic abscess)lProgression to chronic inflammation lLong duration: months to yearslPersistent infection, prolonged exposure to harmful agentsl Prolonged tissue destruction, loss of normal stru
16、cture and function l chronic inflammatory cell Infiltration : Macrophages, Lymphocytes, Plasma cellslpersistent new vessel regeneration and fibroblast proliferation : Resulting in fibrosisPathological ClassificationlAlteration Inflammation (acute)lExudation Inflammation (acute)lProliferation Inflamm
17、ation (chronic)lHemorrhagic InflammationFibrinous Inflammation of Larynx & Trachea due to diphtheriaFibrinous Inflammation of IntestinePseudomembrane (Bacillary Dysentery)Fibrinous Inflammation of Pericardial CavityPulmonary CarnificationAdhesive Pleuritisuppurative or Purulent InflammationAbscess o
18、f Lung Abscess of liver Abscess of cerebrumAbscess of SkinCaused by Staphylococciuperficial SuppurationEmpyema of Fallopian TubeSuppurative meningitis(subarachnoid empyema)Acute phlegmonous appendicitisHemorrhagic InflammationlResolutionlProgression to chronic inflammation lDisseminationLocal spread
19、Lymphatic spreadHematogenous spread Events in the complete resolution of inflammationlReturn to normal vascular permeabilitylRemoval of fluid and proteinlMacrophage pinocytosislPhagocytosis by neutrophilslNecrotic debris by macrophageslEventual exodus by macrophagesulcerMultiple Embolic Abscesses of
20、 KidneyChronic inflammation in lungGranulomatous InflammationlDefinition: Distinctive pattern of chronic inflammation characterized by aggregates of activated macophages that assume a squamous cell-like appearance (epithelioid cell)lMacrophage derivatives: Foamy cell, epithelioid cell, typhoid cell,
21、 Aschoff cell, multinuclear giant cell (Langhans giant cell, foreign body giant cell)Granulomatous InflammationlTuberculosis TuberclelLeparosy Tuberculoid granulomalSyphilis Gumma (syphiloma)lTyphoid Fever Typhoid nodule (typhoid granuloma)lSarcoidosis Noncaseating Epithelioid granulomalCrohn Disease Noncaseating Epithelioid granulomalRheumatic fever Aschoff bodylCat-scratch disease Foreign body giant cells Causes and outcomes of acute and chronic inflammation
