病理學(xué) 炎癥 精選圖片課件

1、Chapter 4：InflammationDepartment of PathologyPeking UniversityHealth Science Center Zheng JieSkin blister result from burningSerous effusion accumulated within and underneath the epidermis of skinFuruncle（癤）Carbuncle（癰)Outlines of inflammationGeneral Considerations Definition; Inflammatory agents; B

2、asic pathological changes of inflammation; Local and systemic manifestations of Inflammation Acute inflammation The process of vascular and cellular events in inflammation, Inflammatory mediatorsThe classification and outcomes of acute inflammation Chronic inflammation Part 1General Considerations C

3、omponents of acute and chronic inflammationInflammatory agentsInfections (bacterial, viral, parasitic) and microbial toxinsPhysical agents (e.g., irradiation, burns) and Trauma (blunt and penetrating) Chemical agents (some environmental chemicals) Ischemic and necrotic tissues Foreign particle (dirt

4、, sutures) Allergic reactionsExudation of plasma proteins Exudate and transudateCause inflammation non-inflammationGross cloudy clearGravity 1.018 30g/L 100/mm3 100/mm3Coagulation + -Mucoprotein + - FeverIncreased acute-phase proteinsLeukocytosisOthers: increased pulse and blood pressure; decreased

5、sweating; rigors; anorexia Systemic manifestations of inflammationPart 2 Acute inflammation Vascular EventsChanges in vascular caliber and flowTransient vasoconstriction of arterioles at the site of injuryVasodilation of precapillary arterioles then increases blood flow to the tissue Increased vascu

6、lar permeabilityThe 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 injury2) Recognition of microbes and dead

7、 tissues3) Removal of the offending agents4) Release of leukocyte products and leukocyte-mediated tissue injuryCellular EventsMargination, rolling and adhesion to endothelium Leukocyte migration through endotheliumChemotaxis and activation1) Recruitment of leukocytes to sites of infection and injury

8、The multiple process of leukocyte migration through blood vessels. Robbins and Cotran Pathologic Basis of Disease 7th edition ChemotaxisAfter extravasating from the blood, leukocytes migrate toward sites of injury along a chemical gradient in a process called Chemotaxis.Chemotactic Factors including

9、 bacterial products, chemokines, C5a, leukotriene B43) Removal of the offending agentsPhagocytosisEngulfmentKilling and degradationRobbins Basic PathologyA. Phagocytosis:AttachmentEngulfmentFusion with lysosomesB. oxygen-dependent bactericidalmechanismInflammatory MediatorFunction of chemical mediat

10、ors: directing the vascular and cellular events in inflammationCell-derived or Plasma-derived mediatorsAct as a complicated network Mediators Sources ActionsHistamineMast cells, basophils, plateletsVasodilation, increased vascular permeability, endothelial activationSerotoninPlateletsVasodilation, i

11、ncreased vascular permeabilityProstaglandinsMast cells, leukocytesVasodilation, pain, feverLeukotrienesMast cells, leukocytesIncreased vascular permeability, chemotaxis, leukocyte adhesion and activationPlatelet-activating factorLeukocytes, mast cellsVasodilation, increased vascular permeability, le

12、ukocyte adhesion, 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 ac

13、tivation (expression 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 C

14、otran Pathologic 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 vas

15、cular permeability, 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 InflammationMediatorsVasodilatio

16、nProstaglandins, 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, ProstaglandinsPainProstaglandi

17、ns, BradykininTissue damageLysosomal enzymes of leukocytes, Reactive oxygen speciesNitric oxide Role of Mediators in Inflammation Inflammatory MediatorVasodilatationVascular permeabilityEDEMAVESOACTIVE MEDIATORSHistamineBradykininC3a C5aLT PGPAFNOTISUE INJURYTraumaIschemiaNeoplasmInfectious agentsFo

18、reign particlePRODUCTION OFINFLAMMATORYMEDIATORSCHEMOTACTIC FACTORS C5a LTB4IL-8, TNFinflammatory cellsACUTE INFLAMMATION Neutrophils, Platelets,Mast cell CHRONICINFLAMMATIONMacrophages,Lymphocytes, Platelets Classification of inflammationClinical classificationPathological classification Clinical C

19、lassification Acute inflammation Chronic inflammationCharacteristics of Acute InflammationShort duration: days to monthsAcute injuries induced by inflammatory agentsExudation: fluid, plasma proteins, neutrophilsAbscess formation Complete resolution can be reached if the injury is limited or short-li

20、vedSevere injury healing by scar formationSpreading : septicemia, pyemia,( metastatic abscess)Progression to chronic inflammationCharacteristics of Chronic Inflammation Long duration: months to yearsPersistent infection, prolonged exposure to harmful agents Prolonged tissue destruction, loss of norm

21、al structure and function chronic inflammatory cell Infiltration : Macrophages, Lymphocytes, Plasma cellspersistent new vessel regeneration and fibroblast proliferation : Resulting in fibrosisPathological ClassificationAlteration Inflammation (acute)Exudation Inflammation (acute)Proliferation Inflam

22、mation (chronic)Viral hepatitis (hepatocyte necrosis)Epidemic Type B Encephalitis (neuronal necrosis) Poliomyelitis (neuronal necrosis) Alteration InflammationAlteration inflammation-Viral hepatitisExudation InflammationSerous InflammationFibrinous InflammaionSuppurative InflammationPhlegnomous Infl

23、ammationSuperficial SuppurationAbscessHemorrhagic InflammationSerous InflammationFeatures: Outpouring of a watery, relatively protein-poor fluid (effusion, with 3%-5% plasma proteins, Albumin) Location: Mucosa, body cavities (peritoneal, pleural & pericardial cavities) , Loose connective tissuesPath

24、ologic changes: Inflammatory edema, blister, hydrops, CatarrhOutcome: complete resolutionSerous InflammationFibrinous InflammationCauses: More severe injuries can result in greater vascular permeability. Larger molecules(esp. fibrinogen)come out through the endothelial cells. Pathologic changes: Eos

25、inophilic meshwork of threads or sometimes as an amorphous coagulum.Location: Mucosa, pericardium , peritonium, body cavities, LungExudation InflammationFibrinous InflammationPathologic changes: Mucosa: Pseudomembraneous Pericardium: Shaggy heartLung: lobar pneumonia Outcome: Resolution: Restore nor

26、mal tissue structureOrganization: scar formation Exudation InflammationFibrinous Inflammation of Larynx & Trachea due to diphtheriaFibrinous Inflammation of IntestinePseudomembrane (Bacillary Dysentery)Fibrinous Inflammation of Pericardial CavityPulmonary CarnificationAdhesive PleuritisSuppurative o

27、r Purulent InflammationFeatures: The presence of large number of neutrophils and varying degrees of tissue necrosis and pus formation. Causes: Pyogenic (pus-producing) bacteriasubclass: Superficial Suppuration, Abscess, Phlegmonous InflammationExudation InflammationAbscessDefinition: Focal localized

28、 collections of purulent inflammatory tissues caused by suppuration buried in a tissue, an organ, or a confined space. Reason: a deep seeding of pyogenic bacteria into a tissueFeatures: Mass of necrotic neutrophils and tissue cells (pus) in the central part, surrounding is cellular proliferation. Ex

29、udation InflammationAbscess of Lung Abscess of liver Abscess of cerebrumExudation InflammationAbscess of Skin Furuncle：the localized suppurative inflammation of haircyst, sebaceous gland & surrounding tissues. Carbuncle：Fusion of quite a few furuncles. Caused by StaphylococciExudation InflammationSu

30、perficial SuppurationLocation: Mucosa, Serosal Membrane. Features: Pus formation, Suppurative Catarrh, Empyema(積膿)Examples: Gall bladder, Fallopian tube, Suppurative meningitis. Exudation InflammationEmpyema of Fallopian TubeSuppurative meningitis(subarachnoid empyema)Phlegmonous InflammationLocatio

31、n: Loose connective tissues: Appendix, Skin. Examples: Phlegmonous appendicitisFeatures: large numbers of neutrophils infiltration. Outcome: heal without sequelaeExudation InflammationAcute phlegmonous appendicitisExudation InflammationErysipelasAn acute disease of the skin and subcutaneous tissue c

32、aused by a species of hemolytic streptococcus and marked by localized inflammation and fever.Also called: Saint Anthonys fireExudation InflammationHemorrhagic Inflammation Features: large numbers of RBC in the exudation. Generally: Its not an independent inflammation In some instances: epidemic hemo

33、rrhagic fever、leptospirosis (鉤端螺旋體病) and plague (鼠疫)Exudation InflammationThe Outcomes of Acute InflammationResolutionProgression to chronic inflammation DisseminationLocal spreadLymphatic spreadHematogenous spread Events in the complete resolution of inflammationReturn to normal vascular permeabili

34、tyRemoval of fluid and proteinMacrophage pinocytosisPhagocytosis by neutrophilsNecrotic debris by macrophagesEventual exodus by macrophagesSinusUlcerFistulaOutcomes of Suppurative InflammationulcerHematogenous Spread of Acute InflammationBacteremia: bacteria enter systemic circulationToxemia ： Toxin

35、s enter systemic circulationSepticemia: bacteria reproduce in systemic circulation, release endotoxin, induce systemic manifestrationsPyemia：sepicemia results from pyegenic bacteria, embolic abscesses occur in multiple organsMultiple Embolic Abscesses of KidneyPart 3 Chronic inflammation Proliferati

36、on inflammation Characterized by cellular proliferation parenchymal cell proliferationmesenchymal cell proliferationlymphoid tissue proliferationgranulomatoue inflammationproliferation of macrophage and its derivativesInflammatory pseudotumorInflammatory polypChronic inflammation in lungGranulomatou

37、s InflammationDefinition: Distinctive pattern of chronic inflammation characterized by aggregates of activated macophages that assume a squamous cell-like appearance (epithelioid cell)Macrophage derivatives: Foamy cell, epithelioid cell, typhoid cell, Aschoff cell, multinuclear giant cell (Langhans giant cell, foreign body giant cell)Granulomatous InflammationTuberculo