Lecture 4-Inflammation and Healing

7/25/2019 Lecture 4-Inflammation and Healing

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Lecture 4Infammation and Repair


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Overview of tissue responsesto injury

Tissue damaged : cellsdie

Acute infammation

Damaging stimuluspersists

Damaging stimulusremoved

Cells cannotregrow

Cells canregrow

Regeneration Healing byrepair

Chronicinfammation

Restorationof normalstructure

and functionScar

formation: lossof specialized

Damaging agentremoved?

o

!es

"ersistent


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Inammation

#ody$s mechanism against damaging agents

on%speci&c immune response

"urposes are 'or:

Clear away dead tissues"rotect against local in'ection

Allow immune system access to the damaged area

Isolate( neutrali)e and remove cause

Initiate healing process

*ither acute or chronic


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Acute inammation vs chronicinammation

Acute

Rapid onset

+asts 'or minutes to

days Characteri)ed by

e,udation o' fuid andprotein 'rom vessels

and emigration o'neutrophils

Results in repairmechanism

hronic

+onger time course-days to years.

Involves di/erent celltypes 0lymphocytesand macrophages.

Tissue repair coe,istwith tissue destruction


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Acute inammation

Cardinal signs: rubor 0red discoloration.( calor0heat.( dolor 0pain.( tumor 0swelling. and loss o''unction

Causes include: in'ection( trauma( physical andchemical agents( necrosis( 'oreign bodies andimmune reactions

1ain 'unctions:23 1ediates local de'enses 4 presence o' acute

infammatory e,udate containing protein( fuid and cells53 Destroys in'ective causative agents 0i' presence.

63 Removes debris 'rom damaged tissue


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7tages:

23 vasodilation(

53 increased vascular permeability(

63 8#C emigration


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!ain "roups of mediatorsinvolved in acute inammation

ellular mediators of acute inammation

7tored Active synthesis

Histamine "rostaglandins( leu9otirnes(platelet activating 'actor(

cyto9ines( ( chemo9ines

#lasma$derived mediators of acute inammation

;inin system #rady9inin

Clotting pathway Activated Hageman 'actor

Thrombolytic system "lasminComplement pathway C6a( C6b( C


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!orpholo"y of acuteinammation

Types o' acute infammation include:

Serous %i&rinous #urulent

Appearanc

e

Relative clear(

watery fuid

=inely

particulate( thic9fuid

"us 0thic9(

white%yellowfuid.

Contents o'fuid

=ew cells( mostinfammation isfuid

1uch moreprotein and cells

eutrophils(protein andnecrotic cells

7een in >iral in'ectionsand burns remic andpostmyocardialin'arctpericarditis

#acterial and'ungal in'ections


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Outcomes of acute inammation'asicdescription

Re(uirements Importantpoints

Resolution Inciting agent isremoved( alldamages arerepaired

rgan is capableo' regenerate

Intact basementmembrane andorgan 'ramewor9

Abscess 8alled o'collection o' pus

#ody cannot rid o/the agent or repairand scarring occur'aster at tissuearound theabscess

Any organ

lcer +oss o' mucosaand deeper tissue3

#ody cannotremove agent

@IT

=istula Anomalous patentconnectionbetween twoorgans

Infammationinvolves 'ullthic9ness o' wallo' organ( duct orblood vessel

Infammatorybowel disease

Chronicinfammation

7car 'ormation Replacement o'tissue arench ma

+oss o' tissue inor a inca able o'


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hronic inammation

"rolonged infammation consisting o' activeinfammation and tissue destruction and repair

Can occur 'ollowing acute infammation and alsoas a low%grade( asymptomatic( prolongedresponse to damaging agent

Causes: viral( persistent microbial in'ection(prolonged e,posure to to,in and autoimmunedys'unction

Cells involved: macrophages and lymphocytes

*,ample: granulomatous 0e3g3tuberculosis(sarcoidosis. Collection o' epitheloid histiocytes( with presence o'

multinucleated giant cells caused by mycobacteria( 'ungi('orei n material( sarcoidosis and silica


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Systemic e)ects ofinammation

"yre,ia: increased in body temperature inducedby pyrogens stimulated by phagocytosis(endoto,ins and immune comple,es

Constitutional symptoms: malaise( anore,ia(nausea

8eight loss: negative nitrogen balance

Reactive hyperplasia o' reticulo%endothelialsystem

Haematological changes: increased *7R(leu9ocytosis( anaemia

Amyloidosis


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Components o' healing Induction o' infammatory process

=ormation o' new blood vessels

"roduction o' e,tracellular matri, including collagen

Tissue remodelling 8ound contracture

Increasing wound strength


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Replacement by scar involves these processes: Angiogenesis

1igration and proli'eration o' &broblasts

Deposition o' e,tracellular matri,

1aturation and reorgani)ation o' &brous tissue

7car 'ormation starts within 5B hours o' onset o'acute infammation A'ter 6 4 < days: granulation tissue is 'ormed

In wee9 5: deposition o' collagen occur3 o edema andinfammatory cells

In 2 month: no infammatory in&ltrate( scar consists o'collagen


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%actors that a)ect woundhealin"

@eneral 'actors include: in'ections( nutritionalde&ciency( glucocorticoid therapy

1echanical 'actors: unintentional reopening o'wound

"oor per'usion: decrease blood supply


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Complications o' healing by scar 'ormation +oss o' 'unction

Contractures and obstructions Results in de'ormity o' oint which restrict oint

movement 0contracture.

7hrin9age o' scar tissue may cause stenosis Adhesions

"revent normal movement o' the structures and maydistorts the tissue

Hypertrophic scar tissue 0e3g3 9eloid.

lceration Due to impaired blood supply

Lecture 4-Inflammation and Healing

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