inflamation 2012

7/23/2019 INFLAMATION 2012

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INFLAMATION

Defnition

Infammation - is the reaction o tissueand

its microcirculation to a pathogenicinsult,

aimed to localize and remove thealtered

cells & harmul actor ollowed by 2

Basic orms o inammation

• Acute exudative inflammation

• Chronic inflammation

• Chronic granulomatous inflammation

Main eatures o acuteinammation

• local process

• genetically determined

• strictly sequentially

• positive influence on tissue

• usually has positive ending

Biological signifcance oinammation

• to eliminate the pathogenic agent,

• to remove injured tissue’s components,

• to repair the tissue.

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)

&"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.

inammation

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.

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!

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

C e l l u l a r s

t a g e

• 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

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

-. 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.

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).

Primaryalteration

c o n d a r y a l t e r a t i o n

+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

#ediators of inflammation (supported of secondary

alteration)

$ellular (leu%ocyte) mediators

! "# !$$

1 l di t

1umoral mediators

(anaphyloto&ins)exudate

($lotting factor )

Eff t f i fl t di t

Effects of inflammatory mediators

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.

Capillary &ed changes in inflammation area

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

1 32 2 4 5 6 7

time$ hours

8. Earlier (transiently) ty"e o "ermeaility.

B. 'mme!iately (longer)ty"e o "ermeaility

C. Delaye! ty"e o"ermeility.

dema is accumulation of fluid within the

e&travascular compartment and interstitial

tissues.

Serous

'i&rinous Purulent

Suppurative

Serosagnuineous

Exudateransudate

ransudate

• is edema fluid ith lo protein

content (specific gravity * ".+",- *

+.+$ mgml

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.

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

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.

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

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

8ecognition 9 attachment to &acteria

acteria

leu:ocyte

: h tt 2 & t i

:acrophages attac2 on &acteria

leu:ocyte

acteria

ca"illary

;acteria digestion

leu:ocyte

acteria

lysosomes

"hagolysosomne

Proliferative events in inflammation(&y <.;=c2er- >.?en2- Ph.@.>eit)

* t+; ;+; +; * <;

"rolieration angiogenesis

macro"hage

frolast

ca"illaries

Tissue recovery

han: you or

your attention

inflamation 2012

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