病理学炎症精选图片课件.ppt

Chapter 4：Inflammation,Department of PathologyPeking UniversityHealth 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 agents; Basic 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,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) 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, sutures) Allergic reactions,The basic pathological changes,Alteration (degeneration, necrosis)Exudation (hallmark, vascular change, leukocyte reaction, inflammatory mediators )Proliferation (parenchymal and strmal cells),Exudation of plasma proteins,Exudate and transudate,Cause inflammation non-inflammationGross cloudy clearGravity 1.018 30g/L 100/mm3 100/mm3Coagulation + -Mucoprotein + -,Local manifestations of Inflammation,rubor (redness)tumor (swelling)calor (heat)dolor (pain),FeverIncreased acute-phase proteinsLeukocytosisOthers: increased pulse and blood pressure; decreased sweating; rigors; anorexia,Systemic manifestations of inflammation,Part 2 Acute inflammation,The process of acute inflammation,Vascular events Cellular events Molecular events,Vascular Events,Changes in vascular caliber and flowTransient vasoconstriction of arterioles at the site of injuryVasodilation of precapillary arterioles then increases blood flow to the tissue Increased vascular permeability,The 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 tissues3) Removal of the offending agents4) Release of leukocyte products and leukocyte-mediated tissue injury,Cellular Events,Margination, rolling and adhesion to endothelium Leukocyte migration through endotheliumChemotaxis and activation,1) Recruitment of leukocytes to sites of infection and injury,The multiple 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 bacterial products, chemokines, C5a, leukotriene B4,2) Recognition of microbes,Leukocyte receptors and responses,3) Removal of the offending agents,PhagocytosisEngulfmentKilling and degradation,Robbins Basic Pathology,A. Phagocytosis:AttachmentEngulfmentFusion with lysosomesB. oxygen-dependent bactericidalmechanism,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 chemical mediators: directing the vascular and cellular events in inflammationCell-derived or Plasma-derived mediatorsAct as a complicated network,Cell-derived mediators,Generation of arachidonic acid metabolites and their roles in inflammation Robbins and Cotran Pathologic Basis of Disease 7th edition,Robbins Basic Pathology,Major effectsof IL-1 and TNF,plasma protein-derived mediators,Interrelationships between the four plasma mediators,Role of Mediators in Inflammation,Inflammatory Mediator,VasodilatationVascular permeability,EDEMA,VESOACTIVE MEDIATORSHistamineBradykininC3a C5aLT PGPAFNO,TISUE INJURYTraumaIschemiaNeoplasmInfectious agentsForeign particle,PRODUCTION OFINFLAMMATORYMEDIATORS,CHEMOTACTIC FACTORS C5a LTB4IL-8, TNF,inflammatory cells,ACUTE INFLAMMATION Neutrophils, Platelets,Mast cell,CHRONICINFLAMMATIONMacrophages,Lymphocytes, Platelets,Classification of inflammation,Clinical classificationPathological classification,Clinical Classification Acute inflammation Chronic inflammation,Characteristics of Acute Inflammation,Short 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-livedSevere injury healing by scar formationSpreading : septicemia, pyemia,( metastatic abscess)Progression to chronic inflammation,Characteristics of Chronic Inflammation,Long duration: months to yearsPersistent infection, prolonged exposure to harmful agents Prolonged tissue destruction, loss of normal structure and function chronic inflammatory cell Infiltration : Macrophages, Lymphocytes, Plasma cellspersistent new vessel regeneration and fibroblast proliferation : Resulting in fibrosis,Pathological Classification,Alteration Inflammation (acute)Exudation Inflammation (acute)Proliferation Inflammation (chronic),Viral hepatitis (hepatocyte necrosis)Epidemic Type B Encephalitis (neuronal necrosis) Poliomyelitis (neuronal necrosis),Alteration Inflammation,Alteration inflammation-Viral hepatitis,Exudation Inflammation,Serous InflammationFibrinous InflammaionSuppurative InflammationPhlegnomous InflammationSuperficial SuppurationAbscessHemorrhagic Inflammation,Serous Inflammation,Features: 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 tissuesPathologic changes: Inflammatory edema, blister, hydrops, CatarrhOutcome: complete resolution,Serous Inflammation,Fibrinous Inflammation,Causes: More severe injuries can result in greater vascular permeability. Larger molecules(esp. fibrinogen)come out through the endothelial cells. Pathologic changes: Eosinophilic meshwork of threads or sometimes as an amorphous coagulum.Location: Mucosa, pericardium , peritonium, body cavities, Lung,Exudation Inflammation,Fibrinous Inflammation,Pathologic changes: Mucosa: Pseudomembraneous Pericardium: Shaggy heartLung: lobar pneumonia Outcome: Resolution: Restore normal tissue structureOrganization: scar formation,Exudation Inflammation,Fibrinous Inflammation of Larynx & Trachea due to diphtheria,Fibrinous Inflammation of IntestinePseudomembrane (Bacillary Dysentery),Fibrinous Inflammation of Pericardial Cavity,Pulmonary Carnification,Adhesive Pleuritis,Suppurative or Purulent Inflammation,Features: 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 Inflammation,Exudation Inflammation,Abscess,Definition: Focal localized 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.,Exudation Inflammation,Abscess of Lung,Abscess of liver Abscess of cerebrum,Exudation Inflammation,Abscess of Skin,Furuncle：the localized suppurative inflammation of haircyst, sebaceous gland & surrounding tissues. Carbuncle：Fusion of quite a few furuncles.,Caused by Staphylococci,Exudation Inflammation,Superficial Suppuration,Location: Mucosa, Serosal Membrane. Features: Pus formation, Suppurative Catarrh, Empyema(积脓)Examples: Gall bladder, Fallopian tube, Suppurative meningitis.,Exudation Inflammation,Empyema of Fallopian Tube,Suppurative meningitis(subarachnoid empyema),Phlegmonous Inflammation,Location: Loose connective tissues: Appendix, Skin. Examples: Phlegmonous appendicitisFeatures: large numbers of neutrophils infiltration. Outcome: heal without sequelae,Exudation Inflammation,Acute phlegmonous appendicitis,Exudation Inflammation,Erysipelas,An acute disease of the skin and subcutaneous tissue caused by a species of hemolytic streptococcus and marked by localized inflammation and fever.Also called: Saint Anthonys fire,Exudation Inflammation,Hemorrhagic Inflammation,Features: large numbers of RBC in the exudation. Generally: Its not an independent inflammation In some instances: epidemic hemorrhagic fever、leptospirosis (钩端螺旋体病) and plague (鼠疫),Exudation Inflammation,The Outcomes of Acute Inflammation,ResolutionProgression to chronic inflammation DisseminationLocal spreadLymphatic spreadHematogenous spread,Events in the complete resolution of inflammationReturn to normal vascular permeabilityRemoval of fluid and proteinMacrophage pinocytosisPhagocytosis by neutrophilsNecrotic debris by macrophagesEventual exodus by macrophages,Sinus,Ulcer,Fistula,Outcomes of Suppurative Inflammation,ulcer,Hematogenous Spread of Acute Inflammation,Bacteremia: bacteria enter systemic circulationToxemia ： Toxins enter systemic circulationSepticemia: bacteria reproduce in systemic circulation, release endotoxin, induce systemic manifestrationsPyemia：sepicemia results from pyegenic bacteria, embolic abscesses occur in multiple organs,Multiple Embolic Abscesses of Kidney,Part 3 Chronic inflammation,Proliferation inflammation,Characterized by cellular proliferation parenchymal cell proliferationmesenchymal cell proliferationlymphoid tissue proliferationgranulomatoue inflammationproliferation of macrophage and its derivativesInflammatory pseudotumorInflammatory polyp,Chronic inflammation in lung,Granulomatous Inflammation,Definition: 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 Inflammation,Tuberculosis TubercleLeparosy Tuberculoid granulomaSyphilis Gumma (syphiloma)Typhoid Fever Typhoid nodule (typhoid granuloma)Sarcoidosis Noncaseating Epithelioid granulomaCrohn Disease Noncaseating Epithelioid granulomaRheumatic fever Aschoff bodyCat-scratch disease,Activated Macrophages in Granulomas,Special type of Macrophage Epithelioid cells: Tuberculosis, Sarcoidosis, Crohn disease, LeparosyTyphoid cells Typhoid feverAschoff cells Rheumatic feverMultinuclear giant cellsLanghans cells : TuberculosisForeign body giant cells: Foreign body granuloma,Chronic Inflammation,Central focus: Caseous necrosis Surrounding: Epithelioid cells Langhans gaint cells Rim: Lymphocytes Fibroblasts,Tubercle/ Tuberculous Granuloma,Foreign body giant cells,Inflammatory Pseudotumor,Tumor-like proliferation of local tissues (parenchymal, stromal, even inflammatory cells) resulting from chronic inflammationIt is not a real tumorOccur in the orbit, lung, liver and spleen,Chronic Inflammation,Inflammatory Polyp,Polypoid lesion of mucosa result from Chronic inflammation composed of mucosal glands, granulation tissue, and inflammatory cells.Commonly seen in nasal, cervical & colorectal mucosa.,Chronic Inflammation,Causes and outcomes of acute and chronic inflammation,