中國醫(yī)科大學病理學英文PPT課件

1、2. Mediators from plasma,Complement S + kinin S + Clotting S,1) kinin system: release of the vasoactive nonapeptide bradykinin,Increases vascular permeability Causes contraction of SM except BV SM Vasodilation Pain,2) Complement System:,(1) Consists of 20 component protein together with their cleava

2、ge products: present as inactive forms( C1C9) (2) Functions : Increase vasopermeability (C3a, C5a) Cause vasodilation (C3a, C5a) Chemotaxist (C5a) Opsonization (C3b),C3a, 5a increase vascular permeability cause vasodilation by releasing histamine from mast cells C5a A powerful chemotactic agent for

3、neutrophils basophils, eosinophils, monocytes Activates the lipoxygenase pathway of AA metabolism in monocytes, neutrophils release of mediators,3) Clotting and fibrinolytic system, Activated clotting system: i) Thrombin and fibrinopeptide: Thrombin promotes leukocyte adhesion fibroblast proliferati

4、on Fibrinopeptide increased V permeability chemotactic activity for leukocytes,ii) Factor Xa increased V permeability leukocyte exudation Activated fibrinolytic system C3 C3a increase v permeability vasodilation Fibrin to fibrin products: increase v permeability,Sources of mediators,3. Summary of in

5、flammatory mediators,Function Major mediators Vasodilation histamine, bradykinin, PGI2, PGE2, NO Permeability histamine, bradykinin, LTB4, C3a, C5a, PAF Chemotaxis LTB4, C5a, cytokins, cationic protein Fever IL-1, IL-2, TNFa, PGE2 Pain PGE2 , bradykinin Tissue damage oxyradical, Lysosomal enzymes ,

6、NO,V. Types and morphology of acute inflammation,Alterative inflammation Degradation, necrosis Acute severe hepatitis, encephalitis b, toxic myocarditis Exudative inflammation Serous Fibrinous Purulent Hemorrhagic Proliferous inflammation Chronic inflammation,Serous inflammation 1. Common sites loos

7、e CT, serosa mucosa and skin 2. Lesions: Serous exudation blood serum (main) secretion of mesothelial C LM albumin: 35% fibrin, neutrophils, epithelial cell,3. Common causes:,Rheumatism, TB involve serosa Burn, cold catarrh 4. Consequence: absorption Harmful sever edema in throat stifle thoracic cav

8、ity pericardial cavity,dysfunction,Serous inflammation of skin,Serous inflammation. Low-power view of a cross-section of a skin blister showing the epidermis separated from the dermis by a focal collection of serous effusion.,The skin blister resulting from a burn or viral infection represents a lar

9、ge accumulation of serous fluid, either within or immediately beneath the epidermis of the skin,Fibrinous inflammation,1. Lesions: Exudates with a large amount of fibrin eosinophilic meshwork of threads or amorphous coagulum Necrotic debris neutrophils 2. Causes bacterial, virus infection intoxicati

10、on: urea, mercury,3. Favor sites and features,(1) Mucosa fibrinous inflammation: Sites upper respiratory tract gastrointestinal tract Feature: pseudomembranous inflammation Fibrin + necrotic tissue + neutrophils gray-white, membrane-shaped Common: bacillary dysentery, diphtheria,Diphtheria of trache

11、a,Larynx 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. Bran-like substances surface the mucosal folds Mucosa appears thickened

12、due to edema Constitutes 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 with fibrinous exudate and form a heavy shaggy coat wit

13、h adhesion between the layers of the pericardium,Fibrinous 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 pericardium. Fine villose form heavy shaggy coat on th

14、 surface.,Fibrinous pericarditis,A pink meshwork of fibrin exudate overlies the pericardial surface.,(3) Lung : lobar pneumonia,the alveolar capillaries appear compressed alveolar spaces: progressive disintegration of neutrophils along with the continued accumulation of fibrin,4. Consequences Resolu

15、tion and absorption Organization: lung carnification heart constrictive pericarditis The 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 lead to scarring. Conversion of the fibrinou

16、s exudate to scar tissue (organization),Suppurative or purulent inflammation,1. 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 leukocytes (mostly neutrophils), the d

17、ebris 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) empyema: pus depo

18、sit in the cavities (gallbladder, appendix),Purulent meningitis,A 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 meningitis,Inflammatory exudates in the widen subarachnoid space

19、. 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: neutrophil

20、s diffuse infiltration,Phlegmonous appendicitis,Appendix is swollen, with yellow-white to tan exudates and hyperemia, rather than a smooth, glistering pale tan serosa suface.,Phlegmonous appendicitis,Mucosa shows ulceration and undermining by an extensive neutrophil exudate. The wall is thickened by

21、 congestion are replaced by monocyte in 2448hs ii) Chronic : LC, PC, monocyte Chemotactic factors: C3a, PDGF, Fibronectin Functions Phagocytosis Tissue damage Fibrosis,The roles of activated macrophages in chronic inflammation. Macrophages are activated by cytokines or by nonimmunologic stimuli. The

22、 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 produce cytokines contribute to fibrosis anaphylactic reaction to

23、drugs (4) Eosinophils: parasite infection,3) 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 cervical polyp intestinal polyp,Smooth mass of tissu

24、e (polyp) with stalks protrudes outwards from the surface of intestine mucosa,Mucosal epithelium, gland & granulation proliferate, and there are lymphocyte & plasma cell infiltration,Nasal polyp,(2) Inflammatory pseudotumor:, Concept: a clear edge, tumor-like mass formed by tissue inflammatory proli

25、feration 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, PC,2. Chronic specific inflammation Granulomatous inflammation,1) Granulomatous inflammation: a distinctive chronic inflammation characteri

26、zed 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 particles

27、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 , fibroblast,Tube

28、rcle,Tubercle,The 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

29、contain 10 or more nuclei arranged peripherally,(2) Foreign body granuloma, Causes : foreign body( talc, suture) Lesions Foreign body Epithelioid cell Foreign body giant cell,Foreign body granuloma,Foreign body gaint cells are seen where there is cholesterol crystal, there r also MC, fibroblasts.,Se

30、ction 4. Local manifestation and general reactions,I. Local manifestation 1. 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 inflammator

31、y mediator (dolor) 5. Loss of function release toxic metabolites and proteases,II. General reactions,1. Fever Exogenous F: toxin, virus, Ag-Ab complex Endogenous F: cytokines IL-1, TNF PG beneficial and harmful 2. Leukocytosis: Acute purulent infla: neutrophils Chronic or virus infection: LC Allergi

32、c disease or parasite: eosinophils left-shift, SLEtyphoid fever virus infection,3. Others M proliferation (liver, spleen, LN) lesions of mesenchymal cells,Section 5. Outcomes of acute inflammation,1) Resolution Complete resolution : Small area: absorptionmorphology and function recovery Incomplete r

33、esolution: Large area: GT fibrosisscar 2) Progression of tissue response to chronic acute chronic (prolonged duration),3) Extension and spreading,Local dissemination Pathogens tissue space or natural tract surrounding tissue or organ TB of kidney ureter bladder TB Lymphatic spread Pathogen lymphatic

34、 lymphatitis lymph node inflammation,Hematogenous spread,(1) Bacteremia: bacteria 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 (h

35、eart, liver, kidney),(3) Septicemia: Strong toxic bacteria propagate in blood and release 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.,Outcomes of acute

36、 inflammation: resolution, healing by fibrosis, or chronic inflammation,病 例 六,病史：男性，40歲，頸部患“癤”，紅、腫、 熱、痛，10天后局部紅腫發(fā)展至手掌大，體溫38，局部手術切開引流。當晚即惡寒、高熱、頭痛，次日體檢發(fā)現(xiàn)病人輕度黃疸，肝脾腫大，體溫39，WBC計數(shù)21.0G/L。 思考題：用所學的炎癥知識，作出病理診 斷并解釋上述臨床表現(xiàn)。,病例六答案,局部臨床表現(xiàn)：紅腫、熱、痛、功能障礙 炎癥全身反應：發(fā)熱39，白細胞改變， 21.0G/L 敗血癥：切開細菌入血；惡寒、高熱、頭 痛、肝脾大，輕度黃疸。,Serous inflammation of skin,Serous inflammation. Low-power view of a cr