logging in or signing up Inflammation robin_vinnu Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Copy Does not support media & animations WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 553 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: October 31, 2010 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... By: roligupta2010 (25 month(s) ago) sir plz allow me to download this ppt as it is very nice Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript CHAPTER 2 : CHAPTER 2 Inflammation (5 OBJECTIVES) 1) (Concept) Understand the chain, progression, or sequence of vascular and cellular events in the histologic evolution of acute inflammation Slide 3: 2) (Rote?) Learn the roles of various “chemical mediators” of acute inflammation 3) Know the three possible outcomes of acute inflammation 4) Visualize the three morphologic patterns of acute inflammation 5) Understand the causes, morphologic patterns, principle cells, minor cells, of chronic and granulomatous inflammation SEQUENCE OF EVENTS : SEQUENCE OF EVENTS NORMAL HISTOLOGY VASODILATATION INCREASED VASCULAR PERMEABILITY LEAKAGE OF EXUDATE MARGINATION, ROLLING, ADHESION TRANSMIGRATION (DIAPEDESIS) CHEMOTAXIS PMN ACTIVATION PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion) TERMINATION 100% RESOLUTION, SCAR, or CHRONIC INFLAMMATION are the three possible outcomes ACUTE INFLAMMATION : ACUTE INFLAMMATION “PROTECTIVE” RESPONSE NON-specific ACUTE INFLAMMATION : ACUTE INFLAMMATION VASCULAR EVENTS CELLULAR EVENTS (PMN or PolyMorphonuclear Neutrophil, Leukocyte?, “POLY”, Neutrophil, Granulocyte, Neutrophilic Granulocyte “MEDIATORS” ACUTE INFLAMMATION : ACUTE INFLAMMATION Neutrophil Polymorphonuclear Leukocyte, PMN, PML “Leukocyte” Granulocyte, Neutrophilic granulocyte “Poly-” Polymorph Slide 8: Rubor Calor Tumor Dolor 5th (functio laesa) HISTORICAL HIGHLIGHTS (Egypt, 3000 BC) STIMULI for acute inflammation : STIMULI for acute inflammation INFECTIOUS PHYSICAL CHEMICAL Tissue Necrosis Foreign Bodies (FBs) Immune “responses”, or “complexes” Vascular Changes : Vascular Changes Changes in Vascular Flow and Caliber Increased Vascular Permeability INCREASED PERMEABILITY : INCREASED PERMEABILITY DILATATION Endothelial “gaps” Direct Injury Leukocyte Injury Transocytosis (endo/exo) New Vessels LEAKAGE OF PROTEINACEOUS FLUID (EXUDATE, NOT TRANSUDATE) : LEAKAGE OF PROTEINACEOUS FLUID (EXUDATE, NOT TRANSUDATE) EXTRAVASATION of PMNs : EXTRAVASATION of PMNs MARGINATION (PMN’s go toward wall) ROLLING (tumbling and HEAPING) ADHESION TRANSMIGRATION (DIAPEDESIS) ADHESION MOLECULES(glycoproteins) affectingADHESION and TRANSMIGRATION : ADHESION MOLECULES(glycoproteins) affectingADHESION and TRANSMIGRATION SECRETINS (from endothelial cells) INTEGRINS (from many cells) CHEMOTAXIS : CHEMOTAXIS PMNs going to the site of “injury” AFTER transmigration LEUKOCYTE“ACTIVATION” : LEUKOCYTE“ACTIVATION” “triggered” by the offending stimuli for PMNs to: 1) Produce eicosanoids (arachidonic acid derivatives) Prostaglandin (and thromboxanes) Leukotrienes Lipoxins 2) Undergo DEGRANULATION 3) Secrete CYTOKINES PHAGOCYTOSIS : PHAGOCYTOSIS RECOGNITION ENGULFMENT KILLING (DEGRADATION/DIGESTION) CHEMICAL MEDIATORS : CHEMICAL MEDIATORS From plasma or cells Have “triggering” stimuli Usually have specific targets Can cause a “cascade” Are short lived CLASSIC MEDIATORS : CLASSIC MEDIATORS HISTAMINE SEROTONIN COMPLEMENT KININS CLOTTING FACTORS EICOSANOIDS NITRIC OXIDE PLATELET ACTIVATING FACTOR (PAF) CYTOKINES /CHEMOKINES LYSOSOME CONSTITUENTS FREE RADICALS NEUROPEPTIDES HISTAMINE : HISTAMINE Mast Cells, basophils POWERFUL Vasodilator Vasoactive “amine” IgE on mast cell SEROTONIN : SEROTONIN (5HT, 5-Hydroxy-Tryptamine) Platelets and EnteroChromaffin Cells Also vasodilatation, but more indirect Evokes N.O. synthetase (a ligase) COMPLEMENT SYSTEM : COMPLEMENT SYSTEM >20 components, in circulating plasma Multiple sites of action, but LYSIS is the underlying theme KININ SYSTEM : KININ SYSTEM BRADYKININ is KEY component, 9 aa’s ALSO from circulating plasma ACTIONS Increased permeability Smooth muscle contraction, NON vascular PAIN CLOTTING FACTORS : CLOTTING FACTORS Also from circulating plasma Coagulation, i.e., production of fibrin Fibrinolysis EICOSANOIDS(ARACHIDONIC ACID DERIVATIVES) : EICOSANOIDS(ARACHIDONIC ACID DERIVATIVES) Part of cell membranes 1) Prostaglandins (incl. Thromboxanes) 2) Leukotrienes 3) Lipoxins (new) MULTIPLE ACTIONS AT MANY LEVELS Prostaglandins(thromboxanes included) : Prostaglandins(thromboxanes included) Pain Fever Clotting Leukotrienes : Leukotrienes Chemotaxis Vasoconstriction Increased Permeability Lipoxins : Lipoxins INHIBIT chemotaxis Vasodilatation Counteract actions of leukotrienes Platelet-Activating Factor(PAF) : Platelet-Activating Factor(PAF) Phospholipid From MANY cells, like eicosanoids ACTIVATE PLATELETS, powerfully CYTOKINES/CHEMOKINES : CYTOKINES/CHEMOKINES CYTOKINES are PROTEINS produced by MANY cells, but usually LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation TNFα, IL-1, by macrophages CHEMOKINES are small proteins which are attractants for PMNs (>40) NITRIC OXIDE : NITRIC OXIDE Potent vasodilator Produced from the action of nitric oxide synthetase from arginine LYSOSOMAL CONSTITUENTS : LYSOSOMAL CONSTITUENTS PRIMARY Also called AZUROPHILIC, or NON-specific Myeloperoxidase Lysozyme (Bact.) Acid Hydrolases SECONDARY Also called SPECIFIC Lactoferrin Lysozyme Alkaline Phosphatase Collagenase FREE RADICALS : FREE RADICALS O2 – (SUPEROXIDE) H2O2 (PEROXIDE) OH- (HYDROXYL RADICAL) VERY VERY DESTRUCTIVE NEUROPEPTIDES : NEUROPEPTIDES Produced in CNS (neurons) SUBSTANCE P NEUROKININ A OUTCOMES OFACUTE INFLAMMATION : OUTCOMES OFACUTE INFLAMMATION 1) 100% complete RESOLUTION 2) SCAR 3)CHRONIC inflammation Morphologic PATTERNSof Acute INFLAMMATION(EXUDATE) : Morphologic PATTERNSof Acute INFLAMMATION(EXUDATE) Serous (watery) Fibrinous (hemorrhagic, rich in FIBRIN) Suppurative (PUS) Ulcerative Slide 39: BLISTER, “Watery”, i.e., SEROUS Slide 40: FIBRINOUS Slide 41: PUS = PURULENT ABSCESS = POCKET OF PUS Slide 42: PURULENT, FIBRINOPURULENT Slide 43: ULCERATIVE SEQUENCE OF EVENTS : SEQUENCE OF EVENTS NORMAL HISTOLOGY VASODILATATION INCREASED VASCULAR PERMEABILITY LEAKAGE OF EXUDATE MARGINATION, ROLLING, ADHESION TRANSMIGRATION (DIAPEDESIS) CHEMOTAXIS PMN ACTIVATION PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion) TERMINATION 100% RESOLUTION, SCAR, or CHRONIC inflammation CHRONIC INFLAMMATION (MONOS) : CHRONIC INFLAMMATION (MONOS) LYMPHOCYTE MONOCYTE MACROPHAGE HISTIOCYTE CAUSES ofCHRONIC INFLAMMATION : CAUSES ofCHRONIC INFLAMMATION 1) PERSISTENCE of Infection 2) PROLONGED EXPOSURE to insult 3) AUTO-IMMUNITY Cellular Players : Cellular Players LYMPHOCYTES MACROPHAGES (aka, HISTIOCYTES) PLASMA CELLS EOSINOPHILS MAST CELLS MORPHOLOGY : MORPHOLOGY INFILTRATION TISSUE DESTRUCTION HEALING GRANULOMASGRANULOMATOUS INFLAMMATION : GRANULOMASGRANULOMATOUS INFLAMMATION 4 COMPONENTS FIBROBLASTS LYMPHS HISTIOS “GIANT” CELLS GRANULOMASGRANULOMATOUS INFLAMMATION : GRANULOMASGRANULOMATOUS INFLAMMATION CASEATING (TB) NON-CASEATING LYMPHATICDRAINAGE : LYMPHATICDRAINAGE SITE REGIONAL LYMPH NODES SYSTEMIC MANIFESTATIONS(NON-SPECIFIC) : SYSTEMIC MANIFESTATIONS(NON-SPECIFIC) FEVER, CHILLS C-Reactive Protein (CRP) “Acute Phase” Reactants Erythrocyte Sedimentation Rate (ESR) increases Leukocytosis Pulse, Blood Pressure Cytokine Effects, e.g., TNF(α), IL-1 Slide 53: NORMAL SPE Serum Protein Electrophoresis In ACUTE Inflammation Alpha-1 & alpha-2 are increased, i.e., “acute phase” reactants. 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Inflammation robin_vinnu Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Copy Does not support media & animations WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 553 Category: Education License: All Rights Reserved Like it (1) Dislike it (0) Added: October 31, 2010 This Presentation is Public Favorites: 0 Presentation Description No description available. Comments Posting comment... By: roligupta2010 (25 month(s) ago) sir plz allow me to download this ppt as it is very nice Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript CHAPTER 2 : CHAPTER 2 Inflammation (5 OBJECTIVES) 1) (Concept) Understand the chain, progression, or sequence of vascular and cellular events in the histologic evolution of acute inflammation Slide 3: 2) (Rote?) Learn the roles of various “chemical mediators” of acute inflammation 3) Know the three possible outcomes of acute inflammation 4) Visualize the three morphologic patterns of acute inflammation 5) Understand the causes, morphologic patterns, principle cells, minor cells, of chronic and granulomatous inflammation SEQUENCE OF EVENTS : SEQUENCE OF EVENTS NORMAL HISTOLOGY VASODILATATION INCREASED VASCULAR PERMEABILITY LEAKAGE OF EXUDATE MARGINATION, ROLLING, ADHESION TRANSMIGRATION (DIAPEDESIS) CHEMOTAXIS PMN ACTIVATION PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion) TERMINATION 100% RESOLUTION, SCAR, or CHRONIC INFLAMMATION are the three possible outcomes ACUTE INFLAMMATION : ACUTE INFLAMMATION “PROTECTIVE” RESPONSE NON-specific ACUTE INFLAMMATION : ACUTE INFLAMMATION VASCULAR EVENTS CELLULAR EVENTS (PMN or PolyMorphonuclear Neutrophil, Leukocyte?, “POLY”, Neutrophil, Granulocyte, Neutrophilic Granulocyte “MEDIATORS” ACUTE INFLAMMATION : ACUTE INFLAMMATION Neutrophil Polymorphonuclear Leukocyte, PMN, PML “Leukocyte” Granulocyte, Neutrophilic granulocyte “Poly-” Polymorph Slide 8: Rubor Calor Tumor Dolor 5th (functio laesa) HISTORICAL HIGHLIGHTS (Egypt, 3000 BC) STIMULI for acute inflammation : STIMULI for acute inflammation INFECTIOUS PHYSICAL CHEMICAL Tissue Necrosis Foreign Bodies (FBs) Immune “responses”, or “complexes” Vascular Changes : Vascular Changes Changes in Vascular Flow and Caliber Increased Vascular Permeability INCREASED PERMEABILITY : INCREASED PERMEABILITY DILATATION Endothelial “gaps” Direct Injury Leukocyte Injury Transocytosis (endo/exo) New Vessels LEAKAGE OF PROTEINACEOUS FLUID (EXUDATE, NOT TRANSUDATE) : LEAKAGE OF PROTEINACEOUS FLUID (EXUDATE, NOT TRANSUDATE) EXTRAVASATION of PMNs : EXTRAVASATION of PMNs MARGINATION (PMN’s go toward wall) ROLLING (tumbling and HEAPING) ADHESION TRANSMIGRATION (DIAPEDESIS) ADHESION MOLECULES(glycoproteins) affectingADHESION and TRANSMIGRATION : ADHESION MOLECULES(glycoproteins) affectingADHESION and TRANSMIGRATION SECRETINS (from endothelial cells) INTEGRINS (from many cells) CHEMOTAXIS : CHEMOTAXIS PMNs going to the site of “injury” AFTER transmigration LEUKOCYTE“ACTIVATION” : LEUKOCYTE“ACTIVATION” “triggered” by the offending stimuli for PMNs to: 1) Produce eicosanoids (arachidonic acid derivatives) Prostaglandin (and thromboxanes) Leukotrienes Lipoxins 2) Undergo DEGRANULATION 3) Secrete CYTOKINES PHAGOCYTOSIS : PHAGOCYTOSIS RECOGNITION ENGULFMENT KILLING (DEGRADATION/DIGESTION) CHEMICAL MEDIATORS : CHEMICAL MEDIATORS From plasma or cells Have “triggering” stimuli Usually have specific targets Can cause a “cascade” Are short lived CLASSIC MEDIATORS : CLASSIC MEDIATORS HISTAMINE SEROTONIN COMPLEMENT KININS CLOTTING FACTORS EICOSANOIDS NITRIC OXIDE PLATELET ACTIVATING FACTOR (PAF) CYTOKINES /CHEMOKINES LYSOSOME CONSTITUENTS FREE RADICALS NEUROPEPTIDES HISTAMINE : HISTAMINE Mast Cells, basophils POWERFUL Vasodilator Vasoactive “amine” IgE on mast cell SEROTONIN : SEROTONIN (5HT, 5-Hydroxy-Tryptamine) Platelets and EnteroChromaffin Cells Also vasodilatation, but more indirect Evokes N.O. synthetase (a ligase) COMPLEMENT SYSTEM : COMPLEMENT SYSTEM >20 components, in circulating plasma Multiple sites of action, but LYSIS is the underlying theme KININ SYSTEM : KININ SYSTEM BRADYKININ is KEY component, 9 aa’s ALSO from circulating plasma ACTIONS Increased permeability Smooth muscle contraction, NON vascular PAIN CLOTTING FACTORS : CLOTTING FACTORS Also from circulating plasma Coagulation, i.e., production of fibrin Fibrinolysis EICOSANOIDS(ARACHIDONIC ACID DERIVATIVES) : EICOSANOIDS(ARACHIDONIC ACID DERIVATIVES) Part of cell membranes 1) Prostaglandins (incl. Thromboxanes) 2) Leukotrienes 3) Lipoxins (new) MULTIPLE ACTIONS AT MANY LEVELS Prostaglandins(thromboxanes included) : Prostaglandins(thromboxanes included) Pain Fever Clotting Leukotrienes : Leukotrienes Chemotaxis Vasoconstriction Increased Permeability Lipoxins : Lipoxins INHIBIT chemotaxis Vasodilatation Counteract actions of leukotrienes Platelet-Activating Factor(PAF) : Platelet-Activating Factor(PAF) Phospholipid From MANY cells, like eicosanoids ACTIVATE PLATELETS, powerfully CYTOKINES/CHEMOKINES : CYTOKINES/CHEMOKINES CYTOKINES are PROTEINS produced by MANY cells, but usually LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation TNFα, IL-1, by macrophages CHEMOKINES are small proteins which are attractants for PMNs (>40) NITRIC OXIDE : NITRIC OXIDE Potent vasodilator Produced from the action of nitric oxide synthetase from arginine LYSOSOMAL CONSTITUENTS : LYSOSOMAL CONSTITUENTS PRIMARY Also called AZUROPHILIC, or NON-specific Myeloperoxidase Lysozyme (Bact.) Acid Hydrolases SECONDARY Also called SPECIFIC Lactoferrin Lysozyme Alkaline Phosphatase Collagenase FREE RADICALS : FREE RADICALS O2 – (SUPEROXIDE) H2O2 (PEROXIDE) OH- (HYDROXYL RADICAL) VERY VERY DESTRUCTIVE NEUROPEPTIDES : NEUROPEPTIDES Produced in CNS (neurons) SUBSTANCE P NEUROKININ A OUTCOMES OFACUTE INFLAMMATION : OUTCOMES OFACUTE INFLAMMATION 1) 100% complete RESOLUTION 2) SCAR 3)CHRONIC inflammation Morphologic PATTERNSof Acute INFLAMMATION(EXUDATE) : Morphologic PATTERNSof Acute INFLAMMATION(EXUDATE) Serous (watery) Fibrinous (hemorrhagic, rich in FIBRIN) Suppurative (PUS) Ulcerative Slide 39: BLISTER, “Watery”, i.e., SEROUS Slide 40: FIBRINOUS Slide 41: PUS = PURULENT ABSCESS = POCKET OF PUS Slide 42: PURULENT, FIBRINOPURULENT Slide 43: ULCERATIVE SEQUENCE OF EVENTS : SEQUENCE OF EVENTS NORMAL HISTOLOGY VASODILATATION INCREASED VASCULAR PERMEABILITY LEAKAGE OF EXUDATE MARGINATION, ROLLING, ADHESION TRANSMIGRATION (DIAPEDESIS) CHEMOTAXIS PMN ACTIVATION PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion) TERMINATION 100% RESOLUTION, SCAR, or CHRONIC inflammation CHRONIC INFLAMMATION (MONOS) : CHRONIC INFLAMMATION (MONOS) LYMPHOCYTE MONOCYTE MACROPHAGE HISTIOCYTE CAUSES ofCHRONIC INFLAMMATION : CAUSES ofCHRONIC INFLAMMATION 1) PERSISTENCE of Infection 2) PROLONGED EXPOSURE to insult 3) AUTO-IMMUNITY Cellular Players : Cellular Players LYMPHOCYTES MACROPHAGES (aka, HISTIOCYTES) PLASMA CELLS EOSINOPHILS MAST CELLS MORPHOLOGY : MORPHOLOGY INFILTRATION TISSUE DESTRUCTION HEALING GRANULOMASGRANULOMATOUS INFLAMMATION : GRANULOMASGRANULOMATOUS INFLAMMATION 4 COMPONENTS FIBROBLASTS LYMPHS HISTIOS “GIANT” CELLS GRANULOMASGRANULOMATOUS INFLAMMATION : GRANULOMASGRANULOMATOUS INFLAMMATION CASEATING (TB) NON-CASEATING LYMPHATICDRAINAGE : LYMPHATICDRAINAGE SITE REGIONAL LYMPH NODES SYSTEMIC MANIFESTATIONS(NON-SPECIFIC) : SYSTEMIC MANIFESTATIONS(NON-SPECIFIC) FEVER, CHILLS C-Reactive Protein (CRP) “Acute Phase” Reactants Erythrocyte Sedimentation Rate (ESR) increases Leukocytosis Pulse, Blood Pressure Cytokine Effects, e.g., TNF(α), IL-1 Slide 53: NORMAL SPE Serum Protein Electrophoresis In ACUTE Inflammation Alpha-1 & alpha-2 are increased, i.e., “acute phase” reactants.