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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. 2) (Rote?) Learn the roles of various “chemical mediators” of acute inflammation

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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

slide3

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

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 inflammation6
ACUTE INFLAMMATION
  • VASCULAR EVENTS
  • CELLULAR EVENTS (PMN or PolyMorphonuclear Neutrophil, Leukocyte?, “POLY”, Neutrophil, Granulocyte, Neutrophilic Granulocyte
  • “MEDIATORS”
acute inflammation7
ACUTE INFLAMMATION

Neutrophil

Polymorphonuclear Leukocyte, PMN, PML

“Leukocyte”

Granulocyte, Neutrophilic granulocyte

“Poly-”

Polymorph

slide8

HISTORICAL

HIGHLIGHTS

(Egypt, 3000 BC)

Rubor

Calor

Tumor

Dolor

5th(functio laesa)

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
extravasation of pmns
EXTRAVASATION of PMNs
  • MARGINATION(PMN’s go toward wall)
  • ROLLING(tumbling and HEAPING)
  • ADHESION
  • TRANSMIGRATION(DIAPEDESIS)
adhesion molecules glycoproteins affecting adhesion 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
HISTAMINE

SEROTONIN

COMPLEMENT

KININS

CLOTTING FACTORS

EICOSANOIDS

NITRIC OXIDE

PLATELET ACTIVATING FACTOR (PAF)

CYTOKINES

/CHEMOKINES

LYSOSOME CONSTITUENTS

FREE RADICALS

NEUROPEPTIDES

CLASSIC MEDIATORS
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) from argenine
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

leukotrienes
Leukotrienes
  • Chemotaxis
  • Vasoconstriction
  • Increased Permeability
lipoxins
Lipoxins
  • INHIBIT chemotaxis
  • Vasodilatation
  • Counteract actions of leukotrienes
p latelet a ctivating f actor 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), e.g., CXC, CC, CX3C, XC families, PF-4, IL-8
n itric o xide
NITRIC OXIDE
  • Potent vasodilator
  • Produced from the action of nitric oxide synthetase from arginine
lysosomal constituents
PRIMARY

Also called AZUROPHILIC, or NON-specific

Myeloperoxidase

Lysozyme (Bact.)

Acid Hydrolases

SECONDARY

Also called SPECIFIC

Lactoferrin

Lysozyme

Alkaline Phosphatase

Collagenase

LYSOSOMAL CONSTITUENTS
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 of acute inflammation
OUTCOMES OFACUTE INFLAMMATION
  • 1) 100% complete RESOLUTION
  • 2) SCAR
  • 3)CHRONIC inflammation
morphologic patterns of acute inflammation exudate
Morphologic PATTERNSof Acute INFLAMMATION(EXUDATE)
  • Serous (watery)
  • Fibrinous (hemorrhagic, rich in FIBRIN)
  • Suppurative (PUS)
  • Ulcerative
slide41

PUS

=

PURULENT

ABSCESS

=

POCKET

OF

PUS

=

NEUTROPHILS

sequence of events44
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)

“MONO”CYTE

MACROPHAGE

HISTIOCYTE

APC

LYMPHOCYTE

causes of chronic 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
granulomas granulomatous inflammation
GRANULOMASGRANULOMATOUS INFLAMMATION

4 COMPONENTS

FIBROBLASTS

LYMPHS

HISTIOS

“GIANT” CELLS

granulomas granulomatous inflammation50
GRANULOMASGRANULOMATOUS INFLAMMATION

CASEATING (TB)

NON-CASEATING

lymphatic drainage
LYMPHATICDRAINAGE
  • SITE REGIONAL LYMPH NODES
systemic manifestations non specific
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
slide53

NORMAL SPE

Serum

Protein

Electrophoresis

In ACUTE

Inflammation

Alpha-1 & alpha-2

are increased, i.e.,

“acute phase”

reactants.