inflamation 2012
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INFLAMATION
Ph.D
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Defnition
Infammation - is the reaction o tissueand
its microcirculation to a pathogenicinsult,
aimed to localize and remove thealtered
cells & harmul actor ollowed by 2
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Basic orms o inammation
• Acute exudative inflammation
• Chronic inflammation
• Chronic granulomatous inflammation
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Main eatures o acuteinammation
• local process
• genetically determined
• strictly sequentially
• positive influence on tissue
• usually has positive ending
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Biological signifcance oinammation
• to eliminate the pathogenic agent,
• to remove injured tissue’s components,
• to repair the tissue.
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Etiology
•Infections factors (toxins)•Trauma (lunt an! "enetrating)
•Physical and chemical agents
(urns or rostite# irra!iation#chemicals)
•Tissue necrosis (rom any cause)
•Foreign bodies (s"linters$ !irt$sutures)
•Immune reactions
( hy"ersensiti%ity)
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&"rea! o 'nammation
•ocal inammation is limite! tocircumscrie! area o tissue inthe %icinity o its "ort o entry.
•Metastatic inammation *transmission o theinammatory "athogens into
other organs an! tissues.•+enerali,e! inammation *"athogen s"rea!s !i-usely
throughout the entire o!y.
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inammation
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he car!inal sym"toms o inammation/
•ruor (redness, hy"eremia)
•calor (local hy"erthermia$ e%er)•tumor (tissue swelling, inammatorytumor)
•!olor (urning "ain)
•lose o unction (unctionalim"airment)
hese eatures corres"on! toinammatory e%ents ovasodilatation, edema, an! tissue
damage.
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Pathogenesis
The stages of inflammation
•Vascular stage (vasodilatation,
increasing o vascular permeability,
epression o vascular receptors!
•Cellular stage (phagocytosis, "#-
dependent cytotoicity!
•&tage o tissue reco%ery ($broplasia,
angiogenesis, cell division%tissue remodeling!
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Phases o acute inammation
Primary alteration
Secondary alteration
Vascular changes (reactions)
Exudation and migration of
leucocytes in site of
inflammation
Cellular proliferation and
tissue regeneration.
V a s c u l a r s t a g
e
C e l l u l a r s
t a g e
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• The acute inflammatory response begins with direct
injury (alteration) or stimulation of cellular or structuralcomponents of a tissue, including:
• ndothelium
• Tissue macrophages and mast cells
• !eutrophils
• "latelets
• #esenchymal cells (e.g., fibroblasts)• "arenchymal cells
$ellular phase
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Endothelial cells are %ey players of inflammation.
• "rovide selective permeability barrier (to e&ogenousand endogenous inflammatory stimuli)'
• egulate leu%ocyte migration (by e&pression of cell
adhesion molecules and receptors)'
• egulate modulate immune responses (by synthesis
release of inflammatory mediators)'
• egulate immune cell proliferation (by secretion of
hematopoietic colony*stimulating factors ($+s)).
- lt ti
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-. lteration
primary alteration / is the result of tissue insult by the harmful factor, that
leads to activation of
secondary alteration via activation of
soluble mediators and
recruitment of inflammatory cells (leucocytes) to the area of damage.
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0uring primary alteration macrophages
and granulocytes mount phagocytic responses (engulf and destroy bacteria).
These are accompanied by the release of
mediators and reactive o&ygen species
into adjacent tissues that may causetissue injury (secondary alteration).
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Primaryalteration
S e
c o n d a r y a l t e r a t i o n
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+econdary alteration begins with releasing of
secondary endogenous mediators ofinflammation:
•1umoral mediators ($omplement sytem, 2inin
sytem, $lotting sytem, ibrinolytic system).
•$ellular mediators (preformed, newly
synthesi3ed (both from leu%ocytes).
# di t f i fl ti ( t d f d
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#ediators of inflammation (supported of secondary
alteration)
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$ellular (leu%ocyte) mediators
! "# !$$
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1 l di t
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1umoral mediators
(anaphyloto&ins)exudate
($lotting factor )
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Eff t f i fl t di t
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Effects of inflammatory mediators
%
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4ascular phase
The vascular changes in inflammation
involve the:• arterioles,
• capillaries,
• venules of microcirculatory bed.
These changes begin almost immediately after
injury and are characteri3ed by vasodilation andchanges in blood flow followed by increased
vascular permeability and leakage of protein-rich
fluid (exudate) to e&travascular tissues.
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Capillary &ed changes in inflammation area
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he ty"es o increasing %ascular "ermeaility insite o inammation (&..0oins)
P e r m
e a i l i t y
m e a s u r i n
g
1 32 2 4 5 6 7
time$ hours
8. Earlier (transiently) ty"e o "ermeaility.
8
B. 'mme!iately (longer)ty"e o "ermeaility
B
C. Delaye! ty"e o"ermeility.
C
9
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dema is accumulation of fluid within the
e&travascular compartment and interstitial
tissues.
Edema
Serous
'i&rinous Purulent
Suppurative
Serosagnuineous
Exudateransudate
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ransudate
• is edema fluid ith lo protein
content (specific gravity * ".+",- *
+.+$ mgml
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Exudate
• is edema fluid ith a high protein
concentration (specific gravity / ".+",)-
hich frequently contains inflammatorycells.
• Exudates are o&served early in acute
inflammatory reactions and are produced &ymild in0uries- such as sun&urn or traumatic
&listers.
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Types of e&udateype Serum Proteins Cells
+erous 5 albumins *
ibrous 5 albumins, fibrin *
"urulent 5 albumins, fibrin leu%ocytes, cell’sdebris
+ero *sangvinous 5 albumins, fibrin leu%ocytes,erythrocytes
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Cellular events1 leu2ocyte transmigration
in vascular lumen1
".marinating-
3.rolling-
$.adhesion to endothelium.through vascular all1
4. transmigration across the endothelium
(diapedesis)
in the tissue1
,. migration to interstitial tissues toard a
chemotactic stimulus.
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he type of emigrating leu2ocyte varies ith1
•Age
•nflammatory response•ype of stimulus.
n most forms of acute inflammation-
neutrophils predominate in the inflammatory
infiltrate during the first 5 to 34 hours- then
are replaced &y monocytes in 34 to 46 hours
Ph t i
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Phagocytosis
is responsi&le for eliminating the in0urious agents
(the ma0or &enefits derived from the accumulation of
leu2ocytes at the inflammatory focus).
Phagocytosis involves the folloing steps11. recognition and attachment of the particle to &e
ingested &y the leu2ocyte7
3. its engulfment - ith su&sequent formation of aphagocytic vacuole7
3. killing or degradation of the ingested material
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8ecognition 9 attachment to &acteria
acteria
leu:ocyte
21
: h tt 2 & t i
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:acrophages attac2 on &acteria
leu:ocyte
acteria
ca"illary
25
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;acteria digestion
leu:ocyte
acteria
lysosomes
"hagolysosomne
27
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Proliferative events in inflammation(&y <.;=c2er- >.?en2- Ph.@.>eit)
* t+; ;+; +; * <;
"rolieration angiogenesis
macro"hage
frolast
5
ca"illaries
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Tissue recovery
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Tissue recovery
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han: you or
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