中国医科大学病理学英文7课件

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 Pain2) Complement System:(1) Consists of 20 component protein together with their cleavage

2、 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 cellsC5a A powerful chemotactic agent for neutr

3、ophils basophils, eosinophils, monocytes Activates the lipoxygenase pathway of AA metabolism in monocytes, neutrophils release of mediators3) Clotting and fibrinolytic system Activated clotting system:i) Thrombin and fibrinopeptide:Thrombin promotes leukocyte adhesion fibroblast proliferationFibrino

4、peptide increased V permeability chemotactic activity for leukocytesSources of mediators3. Summary of inflammatory mediators Function Major mediatorsVasodilation histamine, bradykinin, PGI2, PGE2, NOPermeability histamine, bradykinin, LTB4, C3a, C5a, PAFChemotaxis LTB4, C5a, cytokins, cationic prote

5、in Fever IL-1, IL-2, TNFa, PGE2 Pain PGE2 , bradykininTissue damage oxyradical, Lysosomal enzymes , NOV. Types and morphology of acute inflammationAlterative inflammationDegradation, necrosisAcute severe hepatitis, encephalitis b, toxic myocarditisExudative inflammationSerous Fibrinous Purulent Hemo

6、rrhagic 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 involve serosa Burn

7、, 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 collection of sero

8、us 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 3. Favor sites and features(1) Mucosa fibrinous inflammation: Sites upper respiratory tract gastrointestinal tract Fe

9、ature: pseudomembranous inflammation Fibrin + necrotic tissue + neutrophils gray-white, 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

10、loosely connected with the submucosa of trachea.(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 with adhesion between the layers of the pericardiumFibrino

11、us 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 surface.Fibrinous pericarditis A pink meshwork of fibrin

12、 exudate overlies the pericardial surface. (3) Lung : lobar pneumoniathe alveolar capillaries appear compressed alveolar spaces: progressive disintegration of neutrophils along with the continued accumulation of fibrin 4. Consequences Resolution and absorption Organization: lung carnification heart

13、constrictive pericarditisThe 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 fibrinous exudate to scar tissue (organization) Suppurative or purul

14、ent 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 leukocytes (mostly neutrophils), the debris of dead cells and, in many cases, microbes.2. Causes: St

15、aphylococcus, streptococcus 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 subarachnoid space.Composed of plent

16、y of nutrophils, pus cells, a few monocyte and fibrin.BV are engorged extensively.Phlegmonous 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 a

17、n extensive neutrophil exudate. The wall is thickened by congestion & 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

18、: furuncle, carbuncle Organs: lung, brain, liver, kidney Pathogen: Staphylococcustoxinnecrosis 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 cen

19、ter is walled off by proliferated grayish-white fibrous tissue. Abscess of kidneyYellow 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 accumu

20、lates.Renal mesenchyma engorgement and edema take place at periphery Ulcer1.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 tissueFistula abnoma

21、l connection or passageway between two EC-lined organs that normally do not connect. Hemorrhagic 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 he

22、morrhagic fever Leptospirosis anthraxSection 3. Chronic inflammationI. Etiology and features1. Features: 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

23、 certain microorganisms with lower toxicity Tubercle bacilli ( TB ) Helicobacter pylori (chronic gastritis)2) Prolonged exposure to toxic agentsExogenous: Particulate silica inhaled for prolonged period silicosisEndogenous: Toxic plasma lipid components Atherosclerosis3.Autoimmunity caused by autoan

24、tigens Rheumatoid arthritis, lupus erythematosusII. ClassificationChronic non-specific inflammation Inflammatory polyp Inflammatory pseudotumorChronic specific inflammation ( Granulomatous inflammation ) Infectious granuloma Foreign body granuloma1. Chronic non-specific inflammation1) Morphologic fe

25、atures: (1) Infiltrative cells: LC, PC, MC(2) Proliferation Fibroblast, EC Parenchymal cell (3) Mild degeneration necrosis, exudation(4) Tissue destruction: induced by offending agent or inflammatory cells2) Chronic inflammatory cells (1) Mononuclear phagocyte system: Blood monocyte Tissue macrophag

26、e Connective tissue Liver:Kupffer cells Spleen, LN (sinus histocyte) Lung: alveolar macrophage Consist ofOrgansMaturation of mononuclear phagocytes The age of inflammation:i) Acute : neutrophils predominate during the first 624hs; are replaced by monocyte in 2448hsii) Chronic : LC, PC, monocyte Chem

27、otactic 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 products made by activated macrophages that cause tissue injury and fibrosis are

28、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 drugs (4) Eosinophils: parasite infection3) Some characteristic changes:(1) Inflamm

29、atory polyp: Concept: under the stimulation of inflammatory agents local mucosal epithelium, glands , GT proliferate form protrudent mass Common sites nasal polyp cervical polyp intestinal polypSmooth mass of tissue (polyp) with stalks protrudes outwards from the surface of intestine mucosaMucosal e

30、pithelium, 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 proliferation often occur in eyes and lung . Lesions : In eyes: large amounts of LC proliferat

31、ion In lung: GT, proliferative alveolar epi, M foam C, infiltrative LC, PC2. Chronic specific inflammation Granulomatous inflammation 1) Granulomatous inflammation: a distinctive chronic inflammation characterized by formation of granuloma . Granuloma: in inflammatory foci macrophages proliferate fo

32、rm 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 present some of it to TC cytokines (IL-2, IFN-r) transforming M into epithelioid C and multi

33、nucleate 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 TubercleThe granuloma is referred to as a tubercle. central caseous necrosis appears as p

34、ink, 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 or more nuclei arranged peripherally(2) Foreign body granuloma Causes : foreign body(

35、 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 manifestation and general reactionsI. Local manifestation1. Redness: BV dilating hype

36、remia (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 reactions1. Fe

37、ver 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 fever virus infection3. Others M proliferation (liver, spleen, LN) lesions of mesenchymal cells Section 5. Outcomes of acute inflammation1) ResolutionComplete resolution : Sm