2 CHAPTER CONTENTS Introduction to inflammation Acute inflammation Chronic inflammation
3 INTRODUCTION TO INFLAMMATION CONCEPTIONInflammation is a complex reaction to injurious agents that consists of vascular response, cellular reaction, and systemic reactions.a defensive response fundamentallybe divided into acute inflammation and chronic inflammation
4 INTRODUCTION TO INFLAMMATION CARDINAL CLINICAL SIGNSacute inflammation has 5 cardinal signs:redness (rubor)heat (calor)swellingpain (dolor)loss of functionincreased blood flowto the inflamed areaaccumulation of fluidrelease of chemicals that stimulate nerve endingsa combination of factors
6 INTRODUCTION TO INFLAMMATION SYSTEMIC CLINICAL SIGNSin acute inflammation:A. feverB. changes in the peripheral white blood cell countneutrophils leukocytosisneutrophil nucleus shift to the leftlymphocytosisneutropeniaC. changes in plasma protein levelsthe levels of certain plasma proteins increaseentry of pyrogens and release prostaglandinsbone marrow releaseor productionviral infection
7 neutrophil nucleus shift to the left immaturematureneutrophil nucleus shift to the left
8 ACUTE INFLAMMATION the early response of a tissue to injury the first line of defense against injurynonspecificchanges in the microcirculation:exudation of fluid emigration of leukocytesthe causative factors (6 points)
9 MORPHOLOGIC AND FUNCTIONAL CHANGES the two main components of the acute inflammatory:the microcirculatory responsethe cellular response
10 The microcirculatory response vasodilation and stasisincreased permeabilityexudation of fluid
11 The microcirculatory response A. vasodilation and stasisin the microcirculationa transient vasoconstriction(induced by action of mediators)dilation of arterioles, capillaries, and venules(hyperemia)stasis
12 The microcirculatory response B. increased permeabilityin venules and capillariesactive contraction of actinfilaments in endothelial cellsdirect damage to endothelialcellsleukocyte-mediatedendothelial injurytranscytosis increasedpermeability increase(reversible)
13 The microcirculatory response B. increased permeabilityin venules and capillariesthree phases of increased permeability in acute inflammation:(1) an immediate phase(2) a delayed response(3) a prolonged responsethese permeability changes are effected by various chemical mediators
14 The microcirculatory response C. exudation of fluidexudation: increased passage of fluid out of the microcirculation because of increased vascular permeabilitythe composition of an exudate approaches that of plasma, but rich in proteinsfibrinogen is converted to fibrin rapidlyexudation should be distinguished from transudation
15 Grossly, fibrin is seen on an acute inflamed serosal surface that changes to a rough, yellowish bread andbutter-like surface, covered by fibrin and coagulatedproteins.
16 The microcirculatory response C. exudation of fluidthe functions of exudation:(1) dilute the offending agent(2) cause increased lymphatic flow, conveying noxious agents to the draining lymph nodes to facilitating a protective immune response(3) flood the area with plasma, which contain numerous defensive proteins
17 The cellular response leukocyte infiltration plays an important role in limiting the spread of injuryin defending the host tissueAcute inflammation is characterized by the active emigration of inflammatory cells from the blood into the area of injury.
18 The cellular responseextravasation: the process of the leukocytes from the vessel lumen to the interstitial tissue.3 steps of extravasation :(1) margination, rolling and adhesion to endothelium in the lumen(2) transmigration across the endothelium(3) migration toward the site of injury
19 A. types of cells involved The cellular responseA. types of cells involvedneutrophils(polymorphonuclear leukocytes)phagocytic cell of the macrophage systemlymphocytes and plasma cells
20 The cellular responseB. margination, adhesion and transmigration of neutrophils
21 The cellular response C. emigration of neutrophils take 2-10minutes intercellular junctionsbasement membrane
22 The cellular responseD. chemotactic factorschemotaxis: In the interstitial tissue, neutrophils move toward the site of injury, oriented along a chemical gradient.chemotactic factors: Govern the active emigration of neutrophils and the direction in which they move.
24 The cellular response E. phagocytosis recognition opsonization: the agent has been coated with immunoglobulin or complement factor 3b (opsonins).engulfmentthe agent + opsonins phagosomemicrobial killingphagosome fuses with lysosomes, therefore the enzymes can access to the engulfed microorganism and kill themengulfment
26 The cellular response diapedesis F. erythrocyte the orderly flow of blood is disturbed in the dilated vesselserythrocyte form heavy aggregates and sludgingerythrocyte enter an inflamed area passivelydiapedesishemorrhagic inflammation
28 MEDIATORS OF ACUTE INFLAMMATION A variety of endogenous chemical mediators play some important roles in the modulation of inflammatory response.originated from cells or plasma:cell-derived mediators:sequestered in intracellular granules and synthesized in response to a stimulusplasma-derived mediators:present in precursor form and activated by proteolytic cleavage
29 summary of inflammatory mediators Function Major mediatorsVasodilation HT,histamine, bradykinin ,PGE2Permeability HT,histamine, C3a, C5a, PAFChemotaxis C5a, LTB4, cytokinsFever Cytokines( IL-1, 6, TNF), PGPain PGE2 , bradykininTissue damage Lysosomal enzymes , NO
30 TYPES OF ACUTE INFLAMMATION A. serous inflammationB. fibrinous inflammationC. suppurative (purulent inflammation)D. hemorrhagic inflammation
31 TYPES OF ACUTE INFLAMMATION A. serous inflammationoccur in skin, and in peritoneal, pleural and pericardial cavitiesaccumulation of excessive clear watery fluid with a variable protein contentCatarrhal inflammation is a mild exudative inflammation of a surface mucous membrance without apparent tissue destruction.
34 TYPES OF ACUTE INFLAMMATION B. fibrinous inflammationlarge amounts of fibrinogen pass the vessel wall, and fibrins are formed in the extracellular spacesPseudomembranous inflammation is the fibrinous inflammation occurred on a mucosal surface, and a membranous film consisting mainly of fibrin mixed with necrotic cells appears on the surface of the affected mucosa.
39 TYPES OF ACUTE INFLAMMATION C. suppurative (purulent inflammation)the formation of purulent exudates or pusPus is made up of neutrophils, necrotic cells and edema fluid.Abscess is a localized collection of purulent inflammation accompanied by liquefactive necrosis.
43 TYPES OF ACUTE INFLAMMATION D. hemorrhagic inflammationmarked hemorrhage is the predominant pathological change
44 COURSE OF ACUTE INFLAMMATION A. resolutionB. repairC. suppurationD. chronic inflammation
45 DIAGNOSIS OF ACUTE INFLAMMATION surface structureslocal cardinal signs permit diagnosisinternal organssystemic changes may first manifestrarely, examine a fluid exudates or tissue sample
46 CHRONIC INFLAMMATIONthe sum of the responses mounted by tissue against a persistent injurious agentcommonly showA. immune responseB. phagocytosisC. necrosisD. repair
47 CHRONIC INFLAMMATION the main features include (1) mononuclear cell infiltrationmacrophages play dominant rolls(2) tissue destruction(3) granulation tissue formation and fibrosisbe distinguished from acute inflammation
48 CHRONIC INFLAMMATION IN RESPONSE TO ANTIGENIC INJURIOUS AGENTS mechanismsinjurious agentantigenstissue damageself antigenssome dayschemotactic factorsaccumulation of chronic inflammatory cellsactivated T lymphocytes, plasma cells, macrophages
49 CHRONIC INFLAMMATION IN RESPONSE TO ANTIGENIC INJURIOUS AGENTS morphologic typesA. granulomatous chronic inflammationB. nongranulomatous chronic inflammation
50 granulomatous chronic inflammation a special type of chronic inflammationcharacter: the formation of granulomagranuloma: an aggregate of macrophagestwo types:epithelioid cell granulomaforeign body granuloma
51 granulomatous chronic inflammation characteristic features:the formation of epithelioid cell granulomaepithelioid cell: activated macrophages that appear as large cells with abundant pale, foamy cytoplasmlanghans-type giant cell: derived from fusion of macrophages and characterized by nuclei around the periphery of the cell
53 granulomatous chronic inflammation Granulomas are usually surrounded by lymphocytes, plasma cells, fibroblasts, and collagen.
54 granulomatous chronic inflammation causes(1) When macrophages have successfully phagocytosed the injurious agent but it survives inside them(2) When an active T lymphocyte-mediated cellular immune response occurs
55 granulomatous chronic inflammation changes in affected tissues:granulomas expand and fuse with adjacent granulomas toform largemasses
56 granulomatous chronic inflammation changes in affected tissues:in many infectious granulomas, central caseous necrosis is a common feature
57 granulomatous chronic inflammation caseous necrosis:gross: yellowish-white and resembles crumbly cheesemicroscopic: finely granular, pink, and amorphous
58 nongranulomatous chronic inflammation characteristic features:The accumulation of sensitized lymphocytes, plasma cells, and macrophages in the injured area.These cells are scattered diffusely throughout the tissue.Scattered tissue necrosis and fibrosis are common.
59 nongranulomatous chronic inflammation causes and changes in affected tissues:A. chronic viral infectionsB. chronic autoimmune diseasesC. chronic chemical intoxicationsD. chronic nonviral infectionsE. allergic inflammation and metazoal infections
60 CHRONIC INFLAMMATION IN RESPONSE TO NONANTIGENIC INJURIOUS AGENTS characteristic features:the formation of foreign body granulomaforeign body giant cells: numerous nuclei dispersed throughout the cellforeign material is usually identifiable in the center of the granulomatissue necrosis is not an associated feature(figure 4-19)
62 FUNCTION AND RESULT OF CHRONIC INFLAMMATION function of chronic inflammationserves to contain and remove an injurious agent that is not easily eradicated by the bodydependent on immunologic reactivity:(1) direct killing by activated lymphocytes(2) interaction with antibodies(3) activation of macrophages
63 FUNCTION AND RESULT OF CHRONIC INFLAMMATION associated with tissue necrosis and implies serious illnessassociated fibrosis: a repair mechanism and perhaps another side effect
64 MIXED ACUTE AND CHRONIC INFLAMMATION chronic inflammation may follow acute inflammationor result from repeated bouts of acute inflammationfeatures of both types of inflammation may coexist in certain circumstances
65 CHRONIC SUPPURATIVE INFLAMMATION It is difficult to remove the large amounts of pus associated with chronic suppurative inflammation.The surrounding viable tissue responds with a longstanding inflammatory process in which areas of suppuration alternate with areas of chronic inflammation and fibrosis.
66 CHRONIC SUPPURATIVE INFLAMMATION The difference between an acute and chronic abscess lies in the thickness of the fibrous wall; both form are filled with pus.
68 RECURRENT ACUTE INFLAMMATION if there is predisposing cause, repeated attacks of acute inflammation may occurEach attack of acute inflammation is follwed by incomplete resolution that leads to a progressively increasing number of chronic inflammatory calls and fibrosis.subacute inflammationacute-on-chronic inflammation
69 CLINICAL AND PATHOLOGIC DIAGNOSIS difficultPrecise diagnosis usually requires recourse to a full range of clinical and pathologic studies.table 4-9