11. Inflamasi Akut & Kronik

7/24/2019 11. Inflamasi Akut & Kronik

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"Opportunities are usually"Opportunities are usuallydisguised by hard work, sodisguised by hard work, so

most people don't recognizemost people don't recognizethem."them."

- Ann Landers- Ann Landers


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INFLAMMATIONINFLAMMATIONdr. Al Munawir, M.Kes., Ph.D.

Laboratorium Patologi Anatomi

Fakultas Kedokteran

Universitas Jember


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Introdution!

"In#lame$ % to set #ire.

In#lammationis "d&nami res'onse o#

vasularised tissue to in(ur&.$

Is a 'rotetive res'onse.

)erves to bring de#ense * healingmehanisms to the site o# in(ur&.


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Lewis +ri'le es'onse!

FlushFlush::a'illar& dilatation.

FlareFlare::arteriolar dilatation.WealWeal::e-udation, edema.


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ed, arm * )wollen

/Flare, Flush * eal % Lewis0

+ri'le res'onse


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1astri Uler!


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Lar&ngitis!


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Mouth A'hthus uler


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Aute 2nteritis!


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Pneumonia


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3ardinal )igns o# In#lammation

RuborRubor:: edness % 4&'eraemia.

CalorCalor :: arm % 4&'eraemia.

DolorDolor ::Pain % 5erve, 3hemial med.

TumorTumor::)welling % 2-udation

LossLossofofFunctionFunction::


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In#lammation 6 Mehanism

1. Vaso dilatation

2. Exudation - Edema

3. Emigration of cells

4. Chemotaxis


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Mehanism o# In#lammation!


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5eutro'hil Margination


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7asular hanges


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Pneumonia 6 2-udation


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3hemial Mediators!

3hemial substanes s&nthesised orreleased whih mediate the hanges in

in#lammation.

4istamineb& mast ells 6 vasodilatation.Prostaglandins% 3ause 'ain * #ever.

8rad&kinin6 3auses 'ain.


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Mor'hologi t&'es

Aute!2-udative In#lammation! e-ess #luid. +8 lung.

)u''uration9Purulent % 8aterial 6 neutro'hils

Fibrinous % 'neumonia % #ibrin)erous % e-ess lear #luid % 4eart, lung

4aemorrhagi % b.v.damage 6 anthra-.

3hroni in#lammation! with healing.1rannulomatous % lusters o# e'itheloid: ells

eg. +8, Fungus, Foreign bod&.


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Never let the cometition define !ou.

Instead" !ou have to define !ourself

#ased on a oint of vie$ !ou care

deel! a#out.% om !happel


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In#lammation ;utome

&cuteInflammation

'esolution

ChronicInflammation

scess

(inus)istula

)i#rosis*(car

+lcer

In,ur!

)ungus

Virus

Cancers

.. etc.


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3hroni In#lammation!


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2dema


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)erous In#lammation 6 2##usion


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)erousIn#lammation

6 2##usion


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Fibrinous

In#lammation


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Purulent 6 In#lammation 6 PU)


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Purulent 6In#lammation 6

PU)


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Purulent 6In#lammation 6

PU)


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3hroni

In#lammation!

Lung Absess


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1ranuloma!


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Aute 7s 3hroni

Flush, Flare *eal

Aute

in#lammator& ells6 5eutro'hils

7asular damage

More e-udation

Little or no #ibrosis

Little signs 6Fibrosis,

3hroni

in#lammator& ells% L&m'ho&tes

5eo6vasularisation

5o9less e-udation

Prominent #ibrosis


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/0eole $ho soar" are those

$ho refuse to sit #ac and

$ish things $ould change./

Charles '. ($indoll

&uthor and 0astor


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eat 'edness ($elling 0ain oss f )unc.

+he < 3ardinal )igns o#

Inflammation 35


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4ealing * e'airdr. Al Munawir, M.Kes., Ph.D.

Laboratorium Patologi Anatomi

Fakultas Kedokteran

Universitas Jember


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)tages o# 4ealing!

4emorrhageIn#lammation

1ranulation tissue /so#t allus0)ar % Fibrosis /hard allus0

emodeling * ound strength


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e'air

egeneration o# in(ured tissue b&'arenh&mal ells o# the same t&'e

e'laement b& onnetive tissue

In other wordsegeneration

)ar


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Proli#erative Potential

Labile cells6 ontinuousl& dividing2'idermis, muosal e'ithelium, 1I trat

e'ithelium et

Stable cells6 low level o# re'liation4e'ato&tes, renal tubular e'ithelium,

'anreati aini

Permanent cells6 never divide5erve ells, ardia m&o&tes, skeletal mm


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Pol&'e'tide growth #ators

Most Important Mediators affecting CellGrowth

Present in serum or 'rodued loall&

2-ert 'leiotro'i e##ets= 'roli#eration, ellmigration, di##erentiation, tissue

remodeling

egulate growth o# ells b& ontrollinge-'ression o# genes that regulate ell

'roli#eration


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e'air b& onnetive tissue

;urs when re'air b& 'arenh&malregeneration alone annot be

aom'lished

Involves 'rodution o# Granulation Tissuere'laement o# 'arenh&mal ells with

'roli#erating #ibroblasts and vasular

endothelial ells

3 t # th


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Inflammation-413om'onents o# the 'roess

o# #ibrosis

Angiogenesis 6 5ew vessels budding

#rom old

Fibrosis, onsisting o# emigration and'roli#eration o# #ibroblasts and de'osition

o# 23M

)ar remodeling, tightl& regulated b&'roteases and 'rotease inhibitors


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ound healing

Indution o# aute in#lammator& res'onse

b& an initial in(ur&

Parenh&mal ell regeneration

Migration and 'roli#eration o#

'arenh&mal and onnetive tissue ells


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ound healing /ont>d0

)&nthesis o# 23M 'roteins

emodeling o# 'arenh&mal elements to

restore tissue #untion

emodeling o# onnetive tissue to

ahieve wound strength

I fl i 44


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4ealing b&

First IntentionFoal Disru'tion o#

8asement Membrane

and loss o# onl& a #ew

e'ithelial ells

e.g. )urgial Inision

I fl ti 45


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4ealing b&Secon Intention

Larger in(ur&, absess,

in#artionProess is similar but

esults in muh larger

)ar and then

3;5+A3+I;5

I fl ti 46


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ound )trength

A#ter sutures are removed at one week,wound strength is onl& ?@ o#

unwounded skin /alker> Law0

8& B6C months, wound strength is about@ o# unwounded skin /alker>s Law0

I fl ti 47


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1ranulation tissue

I fl ti 48


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4ealing)kin wound

Inflammation 49


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4ealing 6 )kin )ar

Inflammation 50


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Fators a##eting 4ealing!

S!stemicS!stemicAge

5utrition

7itamin de#.

Immune status

;ther diseases

LocalLocalIn#etion

)iEe or e-tent.

a''osition

8lood su''l&

Mobilit&

Foreign bod&

Inflammation 51


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)ummar&!

4ealing % Proli#eration * Di##erentiation.Labile, )tabe * Permanent ells

)tages o# 4ealing! ?66B6CG.

4ealing b& First or )eond intention.

)kin wound healing 6 bone healing.

Fators a##eting healing % Loal 9

)&stemi


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/Each time !ou are honest and conduct

!ourself $ith honest!" a success force $ill

drive !ou to$ard greater success. Each

time !ou lie" even $ith a little $hite lie"

there are strong forces ushing !ou

to$ard failure./

5oseh (ugarman

&uthor and 6areting (ecialist

11. Inflamasi Akut & Kronik

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