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Learning OutcomesLearning Outcomes
At the end of this lecture, students are ableAt the end of this lecture, students are ableto :to :
1.1. define and list the signs of inflammationdefine and list the signs of inflammation
2.2. explain the vascular and cellular events inexplain the vascular and cellular events inthe acute inflammation.the acute inflammation.
3.3. describe and differentiate in writtendescribe and differentiate in written
between acute and chronic inflammationbetween acute and chronic inflammation4.4. explain the mediators of inflammation.explain the mediators of inflammation.
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What is inflammation?What is inflammation?
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The local response of living mammalian tissuesto injury due to any agent.
Body defense reaction in order to eliminate orlimitthe spread of injurious agent as well as to
remove the consequent necrosed cells andtissues.
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Causes of inflammation;Causes of inflammation;
ii.. Physical agentPhysical agent e.g. mechanical trauma, radiatione.g. mechanical trauma, radiation
etc.etc.
ii.ii. Chemical agentChemical agent e.g. simple chemical poisons,e.g. simple chemical poisons,organic poisonsorganic poisons
iii.iii. InfectiveInfective agentsagents e.g. bacteria, viruses, parasites,e.g. bacteria, viruses, parasites,
their toxinstheir toxins
iv.iv. ImmunologicalImmunological agentsagents e.g. Age.g. Ag--AbAb reaction, cellreaction, cell
mediatedmediated
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Inflammatory response has many players include;Inflammatory response has many players include;
ii.. Circulating cells & plasma proteinsCirculating cells & plasma proteins
ii.ii.Vascular wall cellsVascular wall cells
iii.iii. Cells & extracellular matrix of the surroundingCells & extracellular matrix of the surrounding
connective tissueconnective tissue
Earliest reactions of inflammatory response occursEarliest reactions of inflammatory response occurs
ininVASCULAR CONNECTIVE TISSUEVASCULAR CONNECTIVE TISSUE..
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Stages Of InflammationStages Of Inflammation
INFLAMMATION
ACUTEINFLAMMATION
CHRONICINFLAMMATION
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Acute inflammationAcute inflammation
Short duration & represents the early bodyShort duration & represents the early bodyreaction and usually followed by repairreaction and usually followed by repair
The main features :The main features :
(a)(a) Accumulation of Accumulation offluidfluid && plasmaplasma at theat the
affected siteaffected site
(b)(b) Intravascular activationIntravascular activation of plateletsof platelets
(c)(c) PolymorphonuclearPolymorphonuclear neutrophilsneutrophils asas
inflammatory cellsinflammatory cells
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Chronic InflammationChronic Inflammation
-- longerlonger durationduration andand occursoccurs eithereither ::(a)(a) afterafter thethe causativecausative agentagent ofof acuteacuteinflammationinflammation persistspersists forfor aa longlongtimetime
(b)(b) Stimulus that induces chronicStimulus that induces chronicinflammation from the beginninginflammation from the beginning
-- main features :main features :
presencepresence ofof chronicchronic inflammatoryinflammatory cellscells((lymphocyteslymphocytes,, plasmaplasma cellscells andandmacrophagesmacrophages))
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Signs ofInflammationSigns ofInflammation
The famous 4The famous 4 cardinal signscardinal signs of acuteof acuteinflammation:inflammation:
((ii)) ruborrubor (redness)(redness)(ii)(ii) tumortumor (swelling)(swelling)
(iii)(iii) calorcalor (heat)(heat)
(iv)(iv) dolordolor (pain)(pain)Added latestAdded latest functiofunctio laesalaesa (loss of(loss of
function)function)
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Heat Redness Swelling Pain Loss Of Func.
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((ii)) VASCULAR EVENTSVASCULAR EVENTS
Alteration in the microvasculatureAlteration in the microvasculature(arterioles, capillaries &(arterioles, capillaries & venulesvenules))
Earliest response to tissue injuryEarliest response to tissue injuryAlterations includes:Alterations includes:
(a)(a)haemodynamichaemodynamic changeschanges
(b)(b)changes in vascular permeabilitychanges in vascular permeability
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(a)(a) HaemodynamicHaemodynamic ChangesChanges
Earliest featuresEarliest features ofofinflammatory responseinflammatory responseresult from changes in theresult from changes in the vascular flowvascular flow
andand calibrecalibre of small blood vessels in theof small blood vessels in theinjured tissueinjured tissue
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The sequence of these changes:The sequence of these changes:
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Transient vasoconstriction
Persistent progressive vasodilatation
Local hydrostatic pressure
Slowing or stasis
Leucocytic margination
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LewisLewis Triple Response/ red lineTriple Response/ red line
responseresponse Appears a few second; Capillary & venules
dilatationRed line
Bright reddish appearance appearance/flush surrounding
the red line; Arteriolar dilationFlare
Swelling or oedema of thesurrounding skin occurring dueto transudation of fluid into theextravascular space
wheal
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Triple response
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(b) Altered vascular(b) Altered vascular
permeabilitypermeability Vascular changes begin quickly after the injuryVascular changes begin quickly after the injurybut may develop atbut may develop atvariables ratesvariables rates, depending on, depending on
thethe nature & severity of the original injury.nature & severity of the original injury.
The interchange of fluid between the vascular &The interchange of fluid between the vascular &
extra vascular space results from balance of fluidextra vascular space results from balance of fluid
into the vascular space or out into the tissuesinto the vascular space or out into the tissuesdepend on 4 different types of pressure.depend on 4 different types of pressure.
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Changes vascular permeabilityChanges vascular permeability
Hydrostatic
pressure ?
Oncotic
pressure ?
Osmoticpressure ?
Lymphflow ?
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Fluid interchange between blood andFluid interchange between blood and
extracellular fluid (ECF). (HP = Hydrostaticextracellular fluid (ECF). (HP = Hydrostatic
pressure, OP = Osmotic pressure)pressure, OP = Osmotic pressure)
2020
NOOEDEMA OEDEMA
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MECHANISMS OFINCREASED VASCULARMECHANISMS OFINCREASED VASCULAR
PERMEABILI
TYPERMEABILI
TY
(i)(i) Endothelial cell contractionEndothelial cell contraction
(ii)(ii) Endothelial cell retractionEndothelial cell retraction(iii)(iii) Direct injury to endothelial cellsDirect injury to endothelial cells
(iv)(iv) Endothelial injury mediated by leucocytesEndothelial injury mediated by leucocytes
(v)(v) NeovascularisationNeovascularisation
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ii) CELLULAR EVENTSii) CELLULAR EVENTS
CellularCellular eventsevents;; cellscells ofof thethe acuteacute inflammatoryinflammatoryresponseresponse areare thethe neutrophilsneutrophils,, monocytesmonocytes &&
macrophagesmacrophages..
PolymorphonuclearPolymorphonuclear neutrophilsneutrophils (PMNs)(PMNs)
(within 24 hrs; Life long 24(within 24 hrs; Life long 24--48 hrs)48 hrs)
MonocytesMonocytesMacrophagesMacrophages
(24(24--48 hrs; Survive much longer)48 hrs; Survive much longer)
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TheThe movementsmovements ofof neutrophilsneutrophils outout ofof thethe
vesselsvessels && theirtheir rolerole inin combatcombat cancan bebedivideddivided intointo 55 stepssteps;;
ii.. MarginationMargination ??
ii.ii.AdhesionAdhesion ??
iii.iii. Emigration/Emigration/ diapedesisdiapedesis ??
iv.iv. ChemotaxisChemotaxis ??
v.v. PhagocytosisPhagocytosis && degranulationdegranulation ??
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THE INFLAMMATION PROCESSTHE INFLAMMATION PROCESS
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Neutrophil MarginationNeutrophil Margination
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FATE OF ACUTE INFLAMMATIONFATE OF ACUTE INFLAMMATION
Acute inflammation generally has one ofAcute inflammation generally has one of
FOUR (4) outcomes;FOUR (4) outcomes;
ii.. ResolutionResolution complete return to normal/complete return to normal/
tissue changes are slight and cellular changestissue changes are slight and cellular changesare reversibleare reversible egeg; resolution in lobar; resolution in lobar
pneumoniapneumonia
ii.ii. Healing byHealing by scarrimgscarrimg tissue destruction istissue destruction isextensive, no tissue regeneration; healing byextensive, no tissue regeneration; healing by
fibrosisfibrosis
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iii)iii) SuppurationSuppuration the progression process ofthe progression process of
severe necrosis cause bysevere necrosis cause by pyogenicpyogenic bacteria;bacteria;
neutrophilicneutrophilic infiltration; form aninfiltration; form an abcessabcess;;
abcessabcess organisedorganised by dense fibrous tissueby dense fibrous tissue
and get calcifiedand get calcified
iv)iv) Progression to chronic inflammation mayProgression to chronic inflammation may
follow acute inflammationfollow acute inflammation, although signs, although signsof chronic inflammation may be present atof chronic inflammation may be present at
the onset of injury; healing proceed side bythe onset of injury; healing proceed side byside.side.
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AssessmentAssessment
What is giant cell?What is giant cell?
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ChronicChronic inflammationinflammation;;
prolongedprolonged processprocess inin whichwhich tissuetissuedestructiondestruction andand inflammationinflammation occuroccuratat thethe samesame timetime..
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II) CHRONIC INFLAMMATIONII) CHRONIC INFLAMMATION
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CausedCaused oneone ofof thethe followingfollowing 33 waysways::
ii)) ChronicChronic inflammationinflammation followingfollowing acuteacute
inflammationinflammation thethe tissuetissue destructiondestruction isisextensiveextensive,, oror bacteriabacteria survivesurvive && persistpersist inin
smallsmall numbersnumbers atat thethe sitesite ofof acuteacute inflammationinflammation
ii)ii) RecurrentRecurrent attacksattacks ofof acuteacute inflammationinflammation
repeatedrepeated boutsbouts ofof acuteacute inflammationinflammation egeg;;
repeatedrepeated acuteacute infectioninfection ofof gallbladdergallbladder
chronicchronic cholecystitischolecystitis
iii)iii) StartingStarting dede novonovo infectioninfection withwith organismsorganisms of oflowlow pathogenecitypathogenecity (chronic(chronic fromfrom thethe beginningbeginning))
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GeneralGeneral featuresfeatures ofof ChronicChronic inflammationinflammation::
ii.. InfiltrationInfiltration withwith mononuclearmononuclear cellscells
InfiltratedInfiltrated byby mononuclearmononuclear inflammatoryinflammatory cellscells ::phagocytesphagocytes && lymphoidlymphoid cellscells
phagocytesphagocytes :: circulatingcirculating monocytesmonocytes,, tissuetissue
macrophages,macrophages, epithelioidepithelioid cells,cells, multinucleatedmultinucleated
giantsgiants cellscells
iiii.. TissueTissue destructiondestruction
CentralCentral featurefeature ofof lesionslesions
iiiiii.. ProliferativeProliferative changeschanges
ResultResult ofof necrosis,necrosis, proliferationproliferation ofof smallsmall vesselsvessels
andand fibroblastsfibroblasts;; healinghealing byby fibrosisfibrosis andand collagencollagen
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Types of chronic inflammationTypes of chronic inflammation
NONNON--SPECIFICSPECIFIC
Formation of granulationFormation of granulationtissue and healing bytissue and healing by
fibrosisfibrosis EgEg; Chronic; Chronic osteomyelitisosteomyelitis,,
Chronic ulcerChronic ulcer
SPECIFICSPECIFIC
Injurious agent causes aInjurious agent causes acharacteristiccharacteristic histologichistologic
tissue responsetissue response EgEg; tuberculosis, leprosy,; tuberculosis, leprosy,
syphilissyphilis
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Types of chronic inflammationTypes of chronic inflammation(based on histological classification)(based on histological classification)CHRONIC NONCHRONIC NON--SPECIFICSPECIFIC
INFLAMMATIONINFLAMMATION
CharacterisedCharacterised by:by:
(a) non(a) non--specificspecific
inflammatory cellinflammatory cellinfiltrationinfiltration egeg; chronic; chronicosteomyelitisosteomyelitis, lung, lung abcessabcess
(b) Infiltration by(b) Infiltration by
polymorphs andpolymorphs and abcessabcessformationformation EgEg;;ActinomycosisActinomycosis
CHRONIC GRANULOMATOUSCHRONIC GRANULOMATOUSINFLAMMATIONINFLAMMATION
Formation ofFormation of granulomasgranulomas
EgEg; tuberculosis, leprosy,; tuberculosis, leprosy,
syphilis,syphilis, sarcoidosissarcoidosis
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GranulomatousGranulomatous InflammationInflammation
GranulomatousGranulomatous inflammation; mechanism whereby theinflammation; mechanism whereby the
body deals with certainbody deals with certain indigestibleindigestiblebacteria, fungi, orbacteria, fungi, or
foreign particles.foreign particles.
Examples;Examples;ii.. BacteriaBacteria e.g. Tuberculosis, Leprosye.g. Tuberculosis, Leprosy
ii.ii. ParasiticParasitic e.g.e.g. SchistosomiasisSchistosomiasis
iii.iii. FungaFungal e.g.l e.g. HistoplasmaHistoplasma capsulatumcapsulatum
iv.iv. Inorganic metalsInorganic metals oror dustsdusts e.g. Silicosise.g. Silicosis
v.v. Foreign bodyForeign bodye.g. Vascular grafte.g. Vascular graft
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INJURY(e.g; by M. tuberculosis, talc
Failure to digest agent
Weak acute inflammatory response
Persistence of injurious agent
T cell-mediated immune response Poorly digestible agent
Activation of CD+4 T cells (release oflymphokines IL-1, IL-2. growth factors
IFN- and IFN-)
Monocyte chemotactic factor
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Accumulation of tissue macrophages(Increased recruitment from circulation, local proliferation)
Macrophages activated by IFN-
Transformed to epithelioid cells, giant cells
GRANULOMA
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Granuloma tissueGranuloma tissue
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What is Mediator ???What is Mediator ???
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Mediators Of InflammationMediators Of Inflammation
What are mediators?What are mediators?
ii.. May be circulating in the plasma or may be producedMay be circulating in the plasma or may be produced
locally by cells at the site of inflammation.locally by cells at the site of inflammation.
ii.ii. Induce their effects by binding to specific reactors onInduce their effects by binding to specific reactors on
target cells.target cells.
iii.iii. May stimulate target cells to release secondaryMay stimulate target cells to release secondary effectoreffector
molecules.molecules.iv.iv. May act on only one or a very few targets.May act on only one or a very few targets.
v.v. Function is generallyFunction is generally tighlytighly regulated.regulated.
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2 types of chemical mediators of Acute inflammation;2 types of chemical mediators of Acute inflammation;
i.i. PlasmaPlasma--derived mediatorsderived mediators e.g. kinin system,e.g. kinin system,
coagulation & fibrinolytic system, complementcoagulation & fibrinolytic system, complementsystem.system.
ii.ii. CellCell--derived mediatorsderived mediators e.g. vasoactive amines,e.g. vasoactive amines,
cytokines, platelet activating factor, growth factor.cytokines, platelet activating factor, growth factor.
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Inflammatory cells release mediators such as;Inflammatory cells release mediators such as;
ii.. CytokinesCytokines--((ILIL--8, interferon8, interferon--neutrophilneutrophil))
ii.ii.VasoactiveVasoactive aminesamines--
((histamine,histamine, serotininserotinin-- mast cell,mast cell, basophilbasophil, platelet, platelet))iii.iii. ProstanoidsProstanoids--
((arachidonicarachidonic acidacid metabolicsmetabolics))
iv.iv. Reactive oxygen intermediatesReactive oxygen intermediates--
((released from activatedreleased from activated neutrophilneutrophil))
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If the mediators in the inflammatory response areIf the mediators in the inflammatory response are
successful;successful;
i.i. Invading & infectious agents will be removed.Invading & infectious agents will be removed.
ii.ii. Damaged tissues will be disposed of.Damaged tissues will be disposed of.
iii.iii. New tissue will be induced to form.New tissue will be induced to form.
iv.iv. New blood supply to the area will be established.New blood supply to the area will be established.
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Chronic inflammation cellsChronic inflammation cells
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Chronic InflammationChronic Inflammation Lung AbscessLung Abscess4747
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Morphologic Patterns Of Acute & ChronicMorphologic Patterns Of Acute & Chronic
InflammationInflammation
Serous inflammationSerous inflammation; excessive clear watery; excessive clear watery
fluid with a variable protein content but nofluid with a variable protein content but nofibrin e.g. pleural effusion associated withfibrin e.g. pleural effusion associated with
tuberculosis.tuberculosis.
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Serous InflammationSerous Inflammation -- effusioneffusion
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Serous InflammationSerous Inflammation -- effusioneffusion5050
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Fibrinous inflammationFibrinous inflammation; the formation of; the formation offibrin is striking e.g. in acute pleurisy.fibrin is striking e.g. in acute pleurisy.
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Fibrinous InflammationFibrinous Inflammation5252
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Purulent (Suppurative) inflammationPurulent (Suppurative) inflammation;;production of pus is the main characteristicproduction of pus is the main characteristic
e.g. abscess & acute apendicitis.e.g. abscess & acute apendicitis.
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Purulent InflammationPurulent Inflammation -- PUSPUS
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Purulent InflammationPurulent Inflammation -- PUSPUS
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Ulceration;Ulceration; complicationcomplication of many diseaseof many disease
processprocess
Divided into 2 groups;Divided into 2 groups;i.i. Simple ulcerSimple ulcer
ii.ii. Malignant (cancerous) ulcerMalignant (cancerous) ulcer
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A skin ulcer resulting from infection withA skin ulcer resulting from infection withCorynebacterium diphtheriaeCorynebacterium diphtheriae
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Mouth Apthus UlcerMouth Apthus Ulcer
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Gastric UlcerGastric Ulcer
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"Each time you are honest and conduct
yourself with honesty, a success force will
drive you toward greater success. Eachtime you lie, even with a little white lie,
there are strong forces pushing you towardfailure."
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THANKYOUTHANKYOU
FOR YOURATTENTIONFOR YOURATTENTION