INFLAMATION_biomolsel_2008

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INFLAMATION :INFLAMATION :Cellular ProcessCellular Process

Oleh:Oleh:

dr. Rahma Triliana, S.Ked. M.Kes.dr. Rahma Triliana, S.Ked. M.Kes.

Block : Cellular Moleculer BiologyBlock : Cellular Moleculer BiologyPPD UNISMAPPD UNISMA

Nopember 2008Nopember 2008


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Definitions ofDefinitions of

InflammationInflammation

Its a part of Wound Healing processIts a part of Wound Healing process Protective respons induced byProtective respons induced by

cellular/tissue injury to;cellular/tissue injury to;1.1. minimize the threat to body by: diluting,minimize the threat to body by: diluting,

localising, destroying, & removing of insult orlocalising, destroying, & removing of insult orinjuryinjury

2.2. repairing damagerepairing damage

3.3. restoring normal functionrestoring normal function

Its a dynamic vascular & cellular responseIts a dynamic vascular & cellular responseto insult or injuryto insult or injury can be:can be: beneficial & protective - if regulatedbeneficial & protective - if regulated

injurious - if unregulatedinjurious - if unregulated


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WHEN CELLs EXPOSED TOINJURY


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CAUSESCAUSESmicroorganisms & toxinsmicroorganisms & toxins

parasitesparasites

chemical & biochemical damagechemical & biochemical damage

physical damage:physical damage:heatheat

coldcold

radiationradiation trauma -electrical -mechanicaltrauma -electrical -mechanical

immunologic: types I, III, IVimmunologic: types I, III, IV

hypersensitivityhypersensitivity


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SIGNSIGNComplex ReactionsComplex Reactionsvascularvascularimmunologicalimmunological

cellularcellularClinical SignsClinical SignsRedness/RuborRedness/RuborSwelling/TumorSwelling/TumorHeat/KalorHeat/KalorPain/DolorPain/Dolorloss of function/Functiolesaloss of function/Functiolesa


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TYPESTYPES

Tissue destruction,

Fibrosis

Healing, Abcess

Form., ChronicInflam.

Outcome

s

Mononuclear

(makrophages,lymphocytes, plasmacells), Fibroblast

Macrophages (as

APC), Neutrophils

Major

CellsInvolved

Up tp Months or yearsFew DaysDuration

DelayedImmediateOnset

IFN-& other Cytokines,Growth factors, ROS,

Hydrolytic Enzymes

Vasoactive Amines,eucosanoids

PrimaryMediators

Persistant inflam e.c. nondegradable pathogens,foreign bodies,autoimmune

Pathogens, InjuredTissue

Causative

CHRONICACUTE


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Mediated by:Mediated by:1. Cellular products/cell derived1. Cellular products/cell derived

mediators:mediators: vasoactive aminesvasoactive amines: histamine, 5-: histamine, 5-

hydroxytryptaminehydroxytryptamine mast cells, basophils & plateletsmast cells, basophils & platelets

leads to vasodilatation & increased vascular permeabilityleads to vasodilatation & increased vascular permeability

Cytokines & ChemokinesCytokines & Chemokines (from macrophages &(from macrophages &lymphocytes)lymphocytes) polypeptides leads to increased vascular permeability &polypeptides leads to increased vascular permeability &

dilatationdilatation regulate cellular activity in inflammationregulate cellular activity in inflammation

leukocyte productsleukocyte products (enzymes & O2 radicals)(enzymes & O2 radicals) proteinases leads to degradation of membranes. & collagenproteinases leads to degradation of membranes. & collagen also chemotaxisalso chemotaxis H2O2, O2-, OH. -highly destructiveH2O2, O2-, OH. -highly destructive

products of arachadonic acid metabolismproducts of arachadonic acid metabolismeicosanoidseicosanoids


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EUCOSANOIDFORMATION


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Mediated by..Mediated by..

2. Plasma components/derived2. Plasma components/derived

Mediators:Mediators: kininskinins (e.g. brady kinin)(e.g. brady kinin)

protease-activated plasma proteinsprotease-activated plasma proteins potent vasodilators, increased vasc. permeability & inducepotent vasodilators, increased vasc. permeability & induce

painpain clotting & fibrinolysis systemclotting & fibrinolysis system (fibrinopeptides)(fibrinopeptides)

e.g. fibrinogen, fibrin, thrombin (coagulation system),e.g. fibrinogen, fibrin, thrombin (coagulation system),plasmin (fibrinolysis system), F-XII/Hageman Factor (activeplasmin (fibrinolysis system), F-XII/Hageman Factor (active

by kinin, fibrinolysis & coagulation system)by kinin, fibrinolysis & coagulation system)

chemotactic factors & increased vasc. permeabilitychemotactic factors & increased vasc. permeability

complement cascadecomplement cascade protease-activated plasma proteinsprotease-activated plasma proteins

mediate lytic destruction of cellsmediate lytic destruction of cells chemotaxis, histamine release, increased vascularchemotaxis, histamine release, increased vascular


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EVENTS/STEPSEVENTS/STEPS

ININ

INFLAMMATIONINFLAMMATION


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SEQUENCESEQUENCE

SWELLING

PAIN

- contraction of lining cells- widening of endothelial junctions

- fluid leakage (edema)

-sensory nerve irritation

2)

Permeabilitychanges

LOSS OF

FUNCTION

- local occlution of blood in capillaries &

venules

- congestion

decreased blood flow leads to hypoxia

3)

Hemostasis

REDNESS &

HEAT

- release of vasoactive substances from

damaged & aggregating cells

1)

Changes in

Blood Flow

Clinical

ResponseMechanismEvent


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Sequence.Sequence.

LOSS OF

FUNCTION

connective (scar) tissue formation growth of new blood vessels replacement of destroyed cells

5)

Repair and

Regeneration

PAIN

Chemotaxis: Migration of WBC to area (neutrophilsmononuclear cells) -escape from vessels Phagocytosis:

WBCs indentify, attack, ingest & disposeof foreign matter enzymes, O2 radicals, inflam. Mediators

- removal of noxious agent, tissue debris &

fibrin

leads to further tissue damage

4)

WBC responses-Chemotaxis

-Phagocytosis

Clinical

ResponseMechanismEvent


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WBC RESPONSES


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FLAMMATION CAN BE GIVE LOCAL & SYSTEMIC RESPON


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HARMFULHARMFUL


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HARMFULHARMFULPOTENTIALSPOTENTIALS

Involved in pathogenesis of :Allergic reactions/Hypersensitivities disorder, myopathies,

immune disorders (autoimune diseases), cancer,atherosclerosis (CHD, Stroke), other degenerativesdiseases,

- Anoxia, infarcts, ischemia,shock

- Edema in lungs, abscesses- Inflam. mediators, Cytolysis,

WBC enzymes, free radicals- Arthritis, arteriosclerosis- Pyrexia, secretion- Disuse

- Altered blood supply- Space occupying

lesions- Further tissue damage

- Altered kinetic function- Altered metabolic

functions- Pain

ExamplesResponse

armful effects necessitate therapeutic intervent


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Inflamation in time can resolved in-Chronic Inflammation Inflammation With ChronicSign (Inflammation with partial healing)-Repair/Healing wound Healing-Resolution Rehabilitation/proliferation back to N

state


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Progress of WoundProgress of Wound-Bleeding/cell damage after injury (within hours)-Inflammation process 5 Cardinal sign of Inflammation (within 1 7 Day)-Proliferation Cell & tissue repair process begin (Days Weeks)

-Remodelling Tissue remodelling & getting back to function


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O

UND

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