chapter 2 inflammation (5 objectives) 1) (concept) understand the chain, progression, or sequence of...
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CHAPTER 2Inflammation
(5 OBJECTIVES)1) (Concept) Understand the chain,
progression, or sequence of vascular and cellular events in the histologic evolution of acute inflammation
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2) (Rote?) Learn the roles of various “chemical mediators” of acute inflammation
3) Know the three possible outcomes of acute inflammation
4) Visualize the morphologic patterns of acute inflammation
5) Understand the causes, morphologic patterns, principle cells, minor cells, of chronic and granulomatous inflammation
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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
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ACUTE INFLAMMATION
•“PROTECTIVE” RESPONSE
•NON-specific
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ACUTE INFLAMMATION• VASCULARVASCULAR EVENTS
• CELLULARCELLULAR EVENTS (PMN or PolyMorphonuclear Neutrophil, Leukocyte?, “POLY”, Neutrophil, Granulocyte, Neutrophilic Granulocyte
• ““MEDIATORS”MEDIATORS”
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ACUTE INFLAMMATION
Neutrophil
Polymorphonuclear Leukocyte, PMN, PML
“Leukocyte”
Granulocyte, Neutrophilic granulocyte
“Poly-”
Polymorph
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RuborRubor
CalorCalor
TumorTumor
DolorDolor
5th (functio laesa)
HISTORICAL
HIGHLIGHTS(Egypt, 3000 BC)
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STIMULI for acute inflammation
• INFECTIOUSINFECTIOUS
• PHYSICALPHYSICAL
• CHEMICALCHEMICAL• Tissue Necrosis
• Foreign Bodies (FBs)
• Immune “responses”, or “complexes”
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Vascular Changes• Changes in Vascular Flow
and Caliber
• Increased Vascular Permeability
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INCREASED PERMEABILITY
• DILATATION
• Endothelial “gaps”
• Direct Injury
• Leukocyte Injury
• Transocytosis (endo/exo)
• New Vessels
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LEAKAGE OF PROTEINACEOUS FLUID
(EXUDATEEXUDATE, NOT TRANSUDATE)
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EXTRAVASATION of PMNs
• MARGINATION (PMN’s go toward wall)
• ROLLING (tumbling and HEAPING)
• ADHESION • TRANSMIGRATION
(DIAPEDESIS)
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ADHESION MOLECULES(glycoproteins) affecting
ADHESION and TRANSMIGRATION
• SECRETINS (from endothelial cells)
• INTEGRINS (from many cells)
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CHEMOTAXISPMNs going to the site of “injury”
AFTER transmigration
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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
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PHAGOCYTOSIS• RECOGNITION
• ENGULFMENT
• KILLING (DEGRADATION/DIGESTION)
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CHEMICAL MEDIATORS• From plasma or cellsFrom plasma or cells• Have “triggering” stimuliHave “triggering” stimuli• Usually have specific targetsUsually have specific targets• Can cause a “cascade”Can cause a “cascade”• Are short livedAre short lived
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CLASSIC MEDIATORS• HISTAMINE
• SEROTONIN
• COMPLEMENT
• KININS
• CLOTTING FACTORS
• EICOSANOIDS
• NITRIC OXIDE
• PLATELET ACTIVATING FACTOR (PAF)
• CYTOKINES
• /CHEMOKINES
• LYSOSOME CONSTITUENTS
• FREE RADICALS
• NEUROPEPTIDES
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HISTAMINE• Mast Cells,
basophils• POWERFUL
Vasodilator• Vasoactive
“amine”• IgE on mast
cell
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SEROTONIN• (5HT, 5-Hydroxy-
Tryptamine)
• Platelets and EnteroChromaffin Cells
• Also vasodilatation, but more indirect
• Evokes N.O. synthetase (a ligase) from argenine
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COMPLEMENT SYSTEM• >20
components, in circulating plasma
• Multiple sites of action, but LYSIS is the underlying theme
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KININ SYSTEM• BRADYKININ is KEY component, 9 aa’s• ALSO from circulating plasma• ACTIONS
– Increased permeability– Smooth muscle contraction, NON vascular
–PAINPAIN
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CLOTTING FACTORS
• Also from circulating plasma
• Coagulation, i.e., production of fibrin
• Fibrinolysis
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EICOSANOIDS(ARACHIDONIC ACID DERIVATIVES)
• Part of cell membranes• 1) 1) ProstaglandinsProstaglandins (incl. Thromboxanes)
• 2) 2) LeukotrienesLeukotrienes• 3) 3) LipoxinsLipoxins (new)MULTIPLE ACTIONS AT MANY LEVELS
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Prostaglandins(thromboxanes included)
• Pain
• Fever
• Clotting
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Leukotrienes
• Chemotaxis
• Vasoconstriction
• Increased Permeability
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Lipoxins
• INHIBIT chemotaxis
• Vasodilatation
• Counteract actions of leukotrienes
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Platelet-Activating Factor(PAF)
• Phospholipid
• From MANY cells, like eicosanoids
• ACTIVATE PLATELETS, powerfully
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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), e.g., CXC, CC, CX3C, XC families, PF-4, IL-8
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NITRIC OXIDE• Potent vasodilator
• Produced from the action of nitric oxide synthetase from arginine
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LYSOSOMAL CONSTITUENTS• PRIMARY• Also called
AZUROPHILIC, or NON-specific
• Myeloperoxidase• Lysozyme (Bact.)• Acid Hydrolases
• SECONDARY• Also called SPECIFIC
• Lactoferrin• Lysozyme• Alkaline Phosphatase• Collagenase
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FREE RADICALS• O2 – (SUPEROXIDE)
•H2O2 (PEROXIDE)
•OH- (HYDROXYL RADICAL)
•VERY VERY
DESTRUCTIVE
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NEUROPEPTIDES• Produced in CNS (neurons)
• SUBSTANCE P
• NEUROKININ A
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OUTCOMES OFACUTE INFLAMMATION
• 1) 100% complete RESOLUTION
• 2) SCAR
• 3)CHRONIC inflammation
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Morphologic PATTERNSof Acute INFLAMMATION
(EXUDATE)• SerousSerous (watery)
• FibrinousFibrinous (hemorrhagic, rich in FIBRIN)
• SuppurativeSuppurative (PUS)
• UlcerativeUlcerative
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BLISTER, “Watery”, i.e., SEROUS
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FIBRINOUS
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PUS
=
PURULENT
ABSCESS
=
OF
PUS
=
NEUTROPHILS
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PURULENT, FIBRINOPURULENT
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ULCERATIVE
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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
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CHRONIC INFLAMMATION
(MONOS)
LYMPHOCYTE“MONO”CYTE
MACROPHAGE
HISTIOCYTE
APC
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CAUSES ofCHRONIC INFLAMMATION• 1) PERSISTENCE of Infection
• 2) PROLONGED EXPOSURE to insult
• 3) AUTO-IMMUNITY
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Cellular Players• LYMPHOCYTESLYMPHOCYTES• MACROPHAGESMACROPHAGES (aka, HISTIOCYTES)
• PLASMA CELLS• EOSINOPHILS• MAST CELLS
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MORPHOLOGY• INFILTRATION
• TISSUE DESTRUCTION
• HEALING
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GRANULOMASGRANULOMATOUS INFLAMMATION
4 COMPONENTS
FIBROBLASTS
LYMPHS
HISTIOSHISTIOS
“GIANT” CELLS
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GRANULOMASGRANULOMATOUS INFLAMMATION
CASEATING (TB)
NON-CASEATING
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LYMPHATICDRAINAGE
• SITE REGIONAL LYMPH NODES
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SYSTEMIC MANIFESTATIONS(NON-SPECIFIC)
• FEVER, CHILLS
• C-Reactive Protein (CRP)
• “Acute Phase” Reactants, i.e., α1-α2
• Erythrocyte Sedimentation Rate (ESR) increases
• Leukocytosis
• Pulse, Blood Pressure
• Cytokine Effects, e.g., TNF(α), IL-1
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NORMAL SPE
Serum
Protein
Electrophoresis
In ACUTE
Inflammation
Alpha-1 & alpha-2
are increased, i.e.,
“acute phase”
reactants.