Chapter 4. InflammationSection 1. Introduction
Chapter 4. Inflammation Section 1. Introduction
一.Definition:1. Inflammation: a defensive reaction inlivingtissue withvascularsystemtoinjurious stimuli2.Reaction of BVs is the central linklimiting and killing injured Feliminating and absorbing necrotic T3.The inflammatory responses is closelyinterviewed with the process of repair
一 . Definition: 1. Inflammation: a defensive reaction in living tissue with vascular system to injurious stimuli. 2. Reaction of BVs is the central link limiting and killing injured F eliminating and absorbing necrotic T 3. The inflammatory responses is closely interviewed with the process of repair
4.Significance(1). Beneficial : without inflammationInfections would go uncheckedinjured organs might remain permanentwound would never heal(2).Harmful :hypersensitive reactions to drugs, toxinsfibrinous pericarditis -→constrictive pericarditisfibrous repair → intestinal obstruction
4. Significance (1). Beneficial : without inflammation Infections would go unchecked injured organs might remain permanent wound would never heal (2). Harmful : hypersensitive reactions to drugs, toxins fibrinous pericarditis →constrictive pericarditis fibrous repair → intestinal obstruction
二.Causes and classification(一) C:auses1. Biologic factors:Bac,Virus ,fungi,parasites→the most common2. Chemicalfactors Exogenous :drugs, acidEndogenous :3.Physicalagents:trauma,burn4.Tissue necrosis5.Allergic reaction:GN, TB
二 . Causes and classification (一) Causes 1. Biologic factors:Bac,Virus ,fungi ,parasites →the most common 2. Chemical factors Exogenous : drugs, acid Endogenous : 3. Physical agents: trauma , burn 4. Tissue necrosis 5. Allergic reaction:GN , TB
(二)Clinical types1.Peracuteinflammation(1) sudden onset, lasting for hours or a few days(2)lesion:degeneration,necrosis,exudation2.Acute inflammation() relatively short duration, lasting for a few days(2) lesions: degeneration, necrosis, exudation:neutrophilsinfiltration
(二) Clinical types 1. Peracute inflammation (1) sudden onset, lasting for hours or a few days (2) lesion: degeneration, necrosis, exudation 2. Acute inflammation (1) relatively short duration, lasting for a few days (2) lesions: degeneration, necrosis, exudation: neutrophils infiltration
3. Chronic inflammation()lasting longer duration for a few monthsoryears(2)LesionsrproliferationLLC,PC, Monocyteinfiltration4.Subacuteinflammation(1)between acuteand chronic inflammationderived from acute inflammation
3. Chronic inflammation (1) lasting longer duration for a few months or years (2) Lesions proliferation LC ,PC, Monocyte infiltration 4. Subacute inflammation (1) between acute and chronic inflammation derived from acute inflammation
三.Basicpathologic changes1. Alteration:Degeneration ,necrosis of local tissue cells.Parenchymal Ccellular swellingfatty changecoagulative,liquefactive necrosisMesenchymalCmucoid changeamyloid changefibrinoid necrosishyaline change
三 . Basic pathologic changes 1. Alteration: Degeneration ,necrosis of local tissue cells Parenchymal C cellular swelling fatty change coagulative , liquefactive necrosis Mesenchymal C mucoid change amyloid change fibrinoid necrosis hyaline change
2.Exudation:In inflammatory foci,the escape of fluid,proteins (fibrin),blood cellsfromvascular wallinto interstitial tissue, body cavities orsurface of the body and mucosa3. Proliferation:Parenchymal:epithelium,hepatocyteMesenchymal:fibroblast, EC, histocyte
2. Exudation: In inflammatory foci, the escape of fluid, proteins (fibrin), blood cells from vascular wall into interstitial tissue, body cavities or surface of the body and mucosa 3. Proliferation: Parenchymal : epithelium , hepatocyte Mesenchymal:fibroblast, EC, histocyte
四.Local manifestationlandgeneral reactions(一)Localmanifestation1.Redness: BV dilating hyperemia2.Swelling: congestion, edema ,exudationchronic inflammation →proliferation3. Heat: hyperemia →metabolism→producing heat4.PainswellingN ending pressedinflammatory mediator5.Loss of function
四 . Local manifestation and general reactions (一) Local manifestation 1. Redness: BV dilating →hyperemia 2. Swelling: congestion, edema , exudation chronic inflammation →proliferation 3. Heat: hyperemia →metabolism↑ →producing heat↑ 4. Pain swelling →N ending pressed inflammatory mediator 5. Loss of function
(二)General reactions1.FeverExogenous F: toxin, virus, Ag-Ab complexEndogenous F: cytokines → IL-l, TNF, PG2.Leukocytosis:Acutepurulentinfla:neutrophilsChronic or virus infection: LC个Allergic disease or parasite: eosinophils3. Othersc Anorexia , somnolence ,malaiseMore synthesis of clotting factors
(二) General reactions 1. Fever Exogenous F: toxin, virus, Ag-Ab complex Endogenous F: cytokines → IL-1, TNF, PG 2. Leukocytosis: Acute purulent infla: neutrophils↑ Chronic or virus infection: LC↑ Allergic disease or parasite: eosinophils↑ 3. Others Anorexia , somnolence , malaise More synthesis of clotting factors