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1、中国医科大学病理学英文课件7 Still waters run deep.流静水深流静水深,人静心深人静心深 Where there is life,there is hope。有生命必有希望。有生命必有希望2)Complement System:(1)Consists of 20 component protein together with their cleavage products:present as inactive forms(C1C9)(2)Functions:Increase vasopermeability(C3a,C5a)Cause vasodilation(C3a,C
2、5a)Chemotaxist(C5a)Opsonization(C3b)C3a,5a increase vascular permeability cause vasodilation by releasing histamine from mast cellsC5a A powerful chemotactic agent for neutrophils basophils,eosinophils,monocytes Activates the lipoxygenase pathway of AA metabolism in monocytes,neutrophils release of
3、mediators3)Clotting and fibrinolytic system Activated clotting system:i)Thrombin and fibrinopeptide:Thrombin promotes leukocyte adhesion fibroblast proliferationFibrinopeptide increased V permeability chemotactic activity for leukocytesii)Factor Xa increased V permeability leukocyte exudation Activa
4、ted fibrinolytic system C3 C3a increase v permeability vasodilation Fibrin to fibrin products:increase v permeabilitySources of mediators3.Summary of inflammatory mediators Function Major mediatorsVasodilation histamine,bradykinin,PGI2,PGE2,NOPermeability histamine,bradykinin,LTB4,C3a,C5a,PAFChemota
5、xis LTB4,C5a,cytokins,cationic protein Fever IL-1,IL-2,TNFa,PGE2 Pain PGE2,bradykininTissue damage oxyradical,Lysosomal enzymes,NOV.Types and morphology of acute inflammationAlterative inflammationuDegradation,necrosisuAcute severe hepatitis,encephalitis b,toxic myocarditisExudative inflammationuSer
6、ous uFibrinous uPurulent uHemorrhagic Proliferous inflammation Chronic inflammation Serous inflammation1.Common sites loose CT,serosa mucosa and skin2.Lesions:Serous exudation blood serum(main)secretion of mesothelial C LM albumin:35%fibrin,neutrophils,epithelial cell3.Common causes:Rheumatism,TB in
7、volve serosa Burn,cold catarrh4.Consequence:absorptionHarmful sever edema in throat stifle thoracic cavity pericardial cavity dysfunctionSerous inflammation of skinSerous inflammation.Low-power view of a cross-section of a skin blister showing the epidermis separated from the dermis by a focal colle
8、ction of serous effusion.The skin blister resulting from a burn or viral infection represents a large accumulation of serous fluid,either within or immediately beneath the epidermis of the skin Fibrinous inflammation1.Lesions:Exudates with a large amount of fibrin eosinophilic meshwork of threads or
9、 amorphous coagulum Necrotic debris neutrophils2.Causes bacterial,virus infection intoxication:urea,mercury3.Favor sites and features(1)Mucosa fibrinous inflammation:Sites upper respiratory tract gastrointestinal tract Feature:pseudomembranous inflammation Fibrin+necrotic tissue+neutrophils gray-whi
10、te,membrane-shaped Common:bacillary dysentery,diphtheriaDiphtheria of tracheaLarynx and Treachea all reveal a rough congested mucosa covered by a layer of pseudomembrane.Adhere tightly on laryngeal regions,while loosely connected with the submucosa of trachea.Mucosa of colon is covered by exudates.B
11、ran-like substances surface the mucosal foldsMucosa appears thickened due to edemaConstitutes of the mixture of fibrin,mucus,injured tissue,neutrophils,RBCs,bacilli.(2)Serosa fibrinous inflammation:Sites:pleura,pericardium Feature:fibrinous pericarditis cor villosum Hairy heart,epicardium is covered
12、 with fibrinous exudate and form a heavy shaggy coat with adhesion between the layers of the pericardiumFibrinous pericarditis.Pericardial cavity has been opened to reveal a fibrious pericarditis with strands of stringy pale fibrin between viseral and parietal pericardium.Deposits of fibrin on the p
13、ericardium.Fine villose form heavy shaggy coat on th surface.Fibrinous pericarditis A pink meshwork of fibrin exudate overlies the pericardial surface.(3)Lung:lobar pneumoniathe alveolar capillaries appear compressed alveolar spaces:progressive disintegration of neutrophils along with the continued
14、accumulation of fibrin 4.Consequences Resolution and absorption Organization:lung carnification heart constrictive pericarditislThe process of resolution may restore normal tissue structure,but when the fibrin is not removed,it may stimulate the ingrowth of fibroblasts and blood vessels and thus lea
15、d to scarring.lConversion of the fibrinous exudate to scar tissue(organization)Suppurative or purulent inflammation1.Concept:production of large amounts of pus or purulent exudate consisting of neutrophils necrosis cells and edema fluid.Pus,a purulent exudate,is an inflammatory exudate rich in leuko
16、cytes(mostly neutrophils),the debris of dead cells and,in many cases,microbes.2.Causes:Staphylococcus,streptococcus 3.Types:(1)Surface purulence and empyema Concept:purulent inflammation occurring in mucosa and serosa Features:surface purulence:superfical infiltration of neutrophil(purulent catarrh)
17、empyema:pus deposit in the cavities (gallbladder,appendix)Purulent meningitisA thick layer of suppurative exudate covers the surface of the brain and thickens the leptomeninges.The meningeal vessels are engorged and stand out prominently.Purulent meningitisInflammatory exudates in the widen subarach
18、noid space.Composed of plenty of nutrophils,pus cells,a few monocyte and fibrin.BV are engorged extensively.(2)Phlegmonous inflammation Concept:diffuse purulent inflammation occurring in loose connective tissue Pathogen:hemolytic streptococcus Sites:skin,muscles,appendix Lesion feature:neutrophils d
19、iffuse infiltrationPhlegmonous appendicitisAppendix is swollen,with yellow-white to tan exudates and hyperemia,rather than a smooth,glistering pale tan serosa suface.Phlegmonous appendicitisMucosa shows ulceration and undermining by an extensive neutrophil exudate.The wall is thickened by congestion
20、&edema.Phlegmonous appendicitisNeutrophil extend into and through the wall of the appendix(3)Abscess Concept:localized purulent inflammation accompanied with local tissue necrosis and forming the cavity full of pus.Sites:Skin:furuncle,carbuncle Organs:lung,brain,liver,kidney Pathogen:Staphylococcust
21、oxinnecrosis Results:Small abscess absorption Large abscess become walled off and ultimately replaced by connective tissue Chronic abscess Abscess of liverOn the cutsuface of the liver,an abscess with pus in the center is walled off by proliferated grayish-white fibrous tissue.Abscess of kidneyYello
22、w abscess scattered on the surface of kidney.The infection can reach the kidney by:ascending up the urinary tracthematogenous spread with sepsis Abscess of kidneyFocal renal tissue are necrotic,neutrophils accumulates.Renal mesenchyma engorgement and edema take place at periphery l Ulcer1.Concept:In
23、flammation of skin and mucosa accompanied with superficial necrosis and detachment to form local defect.2.Causes intoxication,trauma vascular obstruction Sinus a sac or cavity in an organ or tissueFistula abnomal connection or passageway between two EC-lined organs that normally do not connect.Hemor
24、rhagic inflammation1.In inflammatory foci,vascular walls severe injured with exudates contain large amounts of RBC 2.Causes:caused by highly virulent organisms such as Waterhouse-Friederichsen S Epidemic hemorrhagic fever Leptospirosis anthraxSection 3.Chronic inflammationI.Etiology and features1.Fe
25、atures:Prolonged duration 1)Follow acute inflammation 2)Frequently begins insidiously often asymptomatic response Rheumatoid arthritis,AS,TB Chronic lung disease2.Causes 1)Persistent infections by certain microorganisms with lower toxicity Tubercle bacilli(TB)Helicobacter pylori(chronic gastritis)2)
26、Prolonged exposure to toxic agentsExogenous:Particulate silica inhaled for prolonged period silicosisEndogenous:Toxic plasma lipid components Atherosclerosis3.Autoimmunity caused by autoantigens Rheumatoid arthritis,lupus erythematosusII.ClassificationlChronic non-specific inflammation Inflammatory
27、polyp Inflammatory pseudotumorlChronic specific inflammation (Granulomatous inflammation)Infectious granuloma Foreign body granuloma1.Chronic non-specific inflammation1)Morphologic features:(1)Infiltrative cells:LC,PC,MC(2)Proliferation Fibroblast,EC Parenchymal cell(3)Mild degeneration necrosis,exu
28、dation(4)Tissue destruction:induced by offending agent or inflammatory cells2)Chronic inflammatory cells (1)Mononuclear phagocyte system:Blood monocyte Tissue macrophage Connective tissue Liver:Kupffer cells Spleen,LN(sinus histocyte)Lung:alveolar macrophage Consist ofOrganslMaturation of mononuclea
29、r phagocytes The age of inflammation:li)Acute:neutrophils predominate duringl the first 624hs;are replaced byl monocyte in 2448hslii)Chronic:LC,PC,monocyte Chemotactic factors:C3a,PDGF,Fibronectin Functions Phagocytosis Tissue damage Fibrosis lThe roles of activated macrophages in chronic inflammati
30、on.lMacrophages are activated by cytokines or by nonimmunologic stimuli.lThe products made by activated macrophages that cause tissue injury and fibrosis are indicated.(2)Lymphocyte:Chemotactic factors:I(V)CAM,lymphotactin Functions:Produce lymphokines(IFN-)(3)Mast cell:Distributed in CT Functions p
31、roduce cytokines contribute to fibrosis anaphylactic reaction to drugs(4)Eosinophils:parasite infection3)Some characteristic changes:(1)Inflammatory polyp:Concept:under the stimulation of inflammatory agents local mucosal epithelium,glands,GT proliferate form protrudent mass Common sites nasal polyp
32、 cervical polyp intestinal polypSmooth mass of tissue(polyp)with stalks protrudes outwards from the surface of intestine mucosaMucosal epithelium,gland&granulation proliferate,and there are lymphocyte&plasma cell infiltration Nasal polyp(2)Inflammatory pseudotumor:Concept:a clear edge,tumor-like mas
33、s formed by tissue inflammatory proliferation often occur in eyes and lung.Lesions:In eyes:large amounts of LC proliferation In lung:GT,proliferative alveolar epi,M foam C,infiltrative LC,PC2.Chronic specific inflammation Granulomatous inflammation 1)Granulomatous inflammation:a distinctive chronic
34、inflammation characterized by formation of granuloma.Granuloma:in inflammatory foci macrophages proliferate form clear nodular focus.2)Types(1)Infectious(immune)granuloma:Concept:caused by insoluble particles that are capable of inducing a cell-mediated immune reaction.Formation:M engulf insoluble p
35、articles present some of it to TC cytokines(IL-2,IFN-r)transforming M into epithelioid C and multinucleate giant C The common diseases:TB,leprosy,rheumatism typhoid fever,syphilis For example:Tuberculosis Central:caseous necrosis Periphery Epithelioid cells Langhans giant cells LC,fibroblastTubercle
36、 TubercleThe granuloma is referred to as a tubercle.central caseous necrosis appears as pink,amorphous granlar debris,loss of all cellular detail.The epitheliod cells have pale pink granular cytoplasm with distinct cell boundaries,Nuclei long and stringy.Epitheliod cells fuse to form LGC contain 10
37、or more nuclei arranged peripherally(2)Foreign body granuloma Causes:foreign body(talc,suture)Lesions Foreign body Epithelioid cell Foreign body giant cellForeign body granulomaForeign body gaint cells are seen where there is cholesterol crystal,there r also MC,fibroblasts.Section 4.Local manifestat
38、ion and general reactionsI.Local manifestation1.Redness:BV dilating hyperemia(rubor)2.Swelling:congestion,edema,exudation chronic inflammation proliferation(tumor)3.Heat:hyperemia metabolism producing heat(calor)4.Pain swelling N ending pressed inflammatory mediator(dolor)5.Loss of function release
39、toxic metabolites and proteases II.General reactions1.Fever Exogenous F:toxin,virus,Ag-Ab complex Endogenous F:cytokines IL-1,TNF PG beneficial and harmful2.Leukocytosis:Acute purulent infla:neutrophils Chronic or virus infection:LC Allergic disease or parasite:eosinophils left-shift,SLEtyphoid feve
40、r virus infection3.Others M proliferation (liver,spleen,LN)lesions of mesenchymal cells Section 5.Outcomes of acute inflammation1)ResolutionlComplete resolution:Small area:absorptionmorphology and function recovery l Incomplete resolution:Large area:GT fibrosisscar2)Progression of tissue response to
41、 chronic acute chronic(prolonged duration)3)Extension and spreadingl Local dissemination Pathogens tissue space or natural tract surrounding tissue or organ TB of kidney ureter bladder TBl Lymphatic spread Pathogen lymphatic lymphatitis lymph node inflammationl Hematogenous spread(1)Bacteremia:bacte
42、ria enter into blood by local focus and can be check out from the blood,without symptoms.(2)Toxemia:bacterial toxin or toxic product enter into blood and accompanied with systemic symptoms and injury of solid organs(heart,liver,kidney)(3)Septicemia:Strong toxic bacteria propagate in blood and releas
43、e toxin to cause severe systemic symptom and lesions.(4)Pyemia:Septicemia cause by pyogenic bacteria accompanied with multiple abscess formation in organs besides manifestation of septicemia.lOutcomes of acute inflammation:resolution,healing by fibrosis,or chronic inflammation 病病 例例 六六病史：病史：男性，男性，40
44、40岁，颈部患岁，颈部患“疖疖”，红、，红、肿、肿、热、痛，热、痛，1010天后局部红肿发展至手天后局部红肿发展至手掌大，体温掌大，体温3838，局部手术切开引流。，局部手术切开引流。当晚即恶寒、高热、头痛，次日体检发当晚即恶寒、高热、头痛，次日体检发现病人轻度黄疸，肝脾肿大，体温现病人轻度黄疸，肝脾肿大，体温3939，WBCWBC计数计数21.0G/L21.0G/L。思考题：思考题：用所学的炎症知识，作出病理诊用所学的炎症知识，作出病理诊 断并解释上述临床表现。断并解释上述临床表现。病例六答案病例六答案局部临床表现：局部临床表现：红肿、热、痛、功能障碍红肿、热、痛、功能障碍炎症全身反应：炎症全身反应：发热发热3939，白细胞改变，白细胞改变，21.0G/L 21.0G/L败血症：败血症：切开细菌入血；恶寒、高热、头切开细菌入血；恶寒、高热、头 痛、肝脾大，轻度黄疸。痛、肝脾大，轻度黄疸。