《中国医科大学病理学英文课件7.ppt》由会员分享,可在线阅读,更多相关《中国医科大学病理学英文课件7.ppt(68页珍藏版)》请在三一文库上搜索。
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 & edema.,Phlegmonous appendicitis,Neutrophil 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, ki
22、dney, Pathogen: Staphylococcustoxinnecrosis Results : Small abscess absorption Large abscess become walled off and ultimately replaced by connective tissue Chronic abscess,Abscess of liver,On the cutsuface of the liver, an abscess with pus in the center is walled off by proliferated grayish-white fi
23、brous tissue.,Abscess of kidney,Yellow abscess scattered on the surface of kidney. The infection can reach the kidney by: ascending up the urinary tract hematogenous spread with sepsis,Abscess of kidney,Focal renal tissue are necrotic, neutrophils accumulates. Renal mesenchyma engorgement and edema
24、take place at periphery,Ulcer,1.Concept: Inflammation 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 tissue Fistula abnomal connection or passageway between two EC-
25、lined organs that normally do not connect.,Hemorrhagic inflammation,1. 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 anthrax,Sec
26、tion 3. Chronic inflammation,I. Etiology and features 1. Features: Prolonged duration 1) Follow acute inflammation 2) Frequently begins insidiously often asymptomatic response Rheumatoid arthritis, AS, TB Chronic lung disease,2. Causes,1) Persistent infections by certain microorganisms with lower to
27、xicity Tubercle bacilli ( TB ) Helicobacter pylori (chronic gastritis),2) Prolonged exposure to toxic agents Exogenous: Particulate silica inhaled for prolonged period silicosis Endogenous: Toxic plasma lipid components Atherosclerosis 3.Autoimmunity caused by autoantigens Rheumatoid arthritis, lupu
28、s erythematosus,II. Classification,Chronic non-specific inflammation Inflammatory polyp Inflammatory pseudotumor Chronic specific inflammation ( Granulomatous inflammation ) Infectious granuloma Foreign body granuloma,1. Chronic non-specific inflammation,1) Morphologic features: (1) Infiltrative cel
29、ls: LC, PC, MC (2) Proliferation Fibroblast, EC Parenchymal cell (3) Mild degeneration necrosis, exudation (4) Tissue destruction: induced by offending agent or inflammatory cells,2) Chronic inflammatory cells,(1) Mononuclear phagocyte system: Blood monocyte Tissue macrophage Connective tissue Liver
30、:Kupffer cells Spleen, LN (sinus histocyte) Lung: alveolar macrophage, Consist of,Organs,Maturation of mononuclear phagocytes, The age of inflammation: i) Acute : neutrophils predominate during the first 624hs; are replaced by monocyte in 2448hs ii) Chronic : LC, PC, monocyte Chemotactic factors: C3
31、a, 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 products made by activated macrophages that cause tissue injury and fibrosis are indicated.,(2) Lymp
32、hocyte:, 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 drugs (4) Eosinophils: parasite infection,3) Some characteristic changes:,(1) Inflammatory polyp: Con
33、cept: 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 tissue (polyp) with stalks protrudes outwards from the surface of intestine mucosa,Mucosal epithelium, gla
34、nd & 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 proliferation often occur in eyes and lung . Lesions : In eyes: large amounts of LC proliferation In lung:
35、 GT, proliferative alveolar epi, M foam C, infiltrative LC, PC,2. Chronic specific inflammation Granulomatous inflammation,1) Granulomatous inflammation: a distinctive chronic inflammation characterized by formation of granuloma . Granuloma: in inflammatory foci macrophages proliferate form clear no
36、dular 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 present some of it to TC cytokines (IL-2, IFN-r) transforming M into epithelioid C and multinucleate
37、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,Tubercle,Tubercle,The granuloma is referred to as a tubercle. central caseous necrosis appears as pink, a
38、morphous 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 or more nuclei arranged peripherally,(2) Foreign body granuloma, Causes : foreign body( ta
39、lc, 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.,Section 4. Local manifestation and general reactions,I. Local manifestation 1. Redness: BV dilating hyp
40、eremia (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 toxic metabolites and proteases,II. General reactions,
41、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 Allergic disease or parasite: eosinophils left-shift, SLEtyphoid fever virus infection,3. Others M prolifera
42、tion (liver, spleen, LN) lesions of mesenchymal cells,Section 5. Outcomes of acute inflammation,1) Resolution Complete resolution : Small area: absorptionmorphology and function recovery Incomplete resolution: Large area: GT fibrosisscar 2) Progression of tissue response to chronic acute chronic (pr
43、olonged 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 lymphatitis lymph node inflammation,Hematogenous spread,(1) Bacteremia: bacteria enter into blood by
44、 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 release toxin to ca
45、use 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 inflammation: resolution, healing by fibrosis, or chronic inflammation,病 例 六,病史:男性,40岁,颈部患“疖”,红、肿、 热、痛,10天后局部红肿发展至手掌大,体温38,局部手术切开引流。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39,WBC计数21.0G/L。 思考题:用所学的炎症知识,作出病理诊 断并解释上述临床表现。,病例六答案,局部临床表现:红肿、热、痛、功能障碍 炎症全身反应:发热39,白细胞改变, 21.0G/L 败血症:切开细菌入血;恶寒、高热、头 痛、肝脾大,轻度黄疸。,
链接地址:https://www.31doc.com/p-3096066.html