InflammationInflammation

Inflammation Inflammation

Body’s most important defence mechanismBody’s most important defence mechanismIt is the response of living, vascularized tissue to an It is the response of living, vascularized tissue to an

injurious agentinjurious agent

1/ Localise and remove the injurious agent.2/ Protects against infections3/ Restore the normal structure.

Significance

May cause tissue damage

Adverse effects

Infllamed tissue are named with a suffix Infllamed tissue are named with a suffix ‘ITIS’‘ITIS’

Inflammation of appendix---------Appendicitis.Inflammation of appendix---------Appendicitis.

Inflammation of liver----------------Hepatitis.Inflammation of liver----------------Hepatitis.

Inflammation of gall bladder------CholecystitisInflammation of gall bladder------Cholecystitis

Causes of InflammationCauses of Inflammation

microbial Infectionsmicrobial Infections – pyogenic bacteria, virus, fungi – pyogenic bacteria, virus, fungihypersensitivity reactionshypersensitivity reactions – injury due to antigen- – injury due to antigen-antibody reactionsantibody reactionsphysical agentsphysical agents – trauma, radiation, heat, cold – trauma, radiation, heat, coldChemicals Chemicals – acids, alkalis– acids, alkalisMechanical agents: Mechanical agents: Wounds, fracture, crushing Wounds, fracture, crushing injuries, injuries,

Effects of InflammationEffects of Inflammation

When the irritant reaches the tissues, it When the irritant reaches the tissues, it causes injury to the cells, resulting in causes injury to the cells, resulting in release of various chemical substances release of various chemical substances called called mediators.mediators.

These mediators initiate either These mediators initiate either locallocal or or generalgeneral effects. effects.

Local EffectsLocal Effects

Vascular changes.Vascular changes.

Very important feature of inflammation especially of acute type.

Takes place in small blood vessels, and aninflammatory exudate comes out from inside the blood vessels to the area involved in order to attack the irritant.

Systemic ChangesSystemic Changes

Fever:Fever:

Changes in blood cells: Changes in blood cells: – Leukocytosis.Leukocytosis.

Neutrophils--pyogenic or suppurative inflammationNeutrophils--pyogenic or suppurative inflammation

Eosinophils—parasitic infections, allergiesEosinophils—parasitic infections, allergies

Lymphocytes—chronic infections, viralLymphocytes—chronic infections, viral

– Some degree of anemia due to toxic depression of Some degree of anemia due to toxic depression of bone marrow. bone marrow.

Changes in organs:Changes in organs:– Hyperplasia of mononuclear-phagocyte system Hyperplasia of mononuclear-phagocyte system

Redness Redness

SwellingSwelling

Heat Heat

Pain Pain

Loss of functionLoss of function

Signs of Inflammation

ACUTE:ACUTE: – Almost completely stereotyped.Almost completely stereotyped.– Over minutes to a few days.Over minutes to a few days.– Blood vessels dilate and leakBlood vessels dilate and leak– Neutrophils enter the surrounding tissuesNeutrophils enter the surrounding tissues

CHRONICCHRONIC– More variableMore variable– Variable participation by lymphocytes, plasma Variable participation by lymphocytes, plasma

cells, macrophages and healing cells (fibroblasts cells, macrophages and healing cells (fibroblasts and angioblastsand angioblasts) )

TYPES

ACUTE INFLAMMATIONACUTE INFLAMMATION

Immediate and early response to an injurious Immediate and early response to an injurious agent.agent.

Vasodilation .Vasodilation .

Vascular Leakage and Edema.Vascular Leakage and Edema.

Leukoctic emigration, mostly PMNLLeukoctic emigration, mostly PMNL ( macrophages appear later).( macrophages appear later).

Lasts for a few hours or days and then resolves.Lasts for a few hours or days and then resolves.

Little or no permanent damage.Little or no permanent damage.

Neutrophil

VASODILATATIONVASODILATATIONBrief arterial vasoconstriction followed by Brief arterial vasoconstriction followed by vasodilatationvasodilatation

Accounts for warmth and rednessAccounts for warmth and redness

Opens microvascular beds and leads to Opens microvascular beds and leads to increased blood flow into damaged tissue.increased blood flow into damaged tissue.

Increased intravascular hydrostatic Increased intravascular hydrostatic pressure causes early transudate( protein pressure causes early transudate( protein poor filtrate of plasma) into interstitium poor filtrate of plasma) into interstitium ( vascular permeability still not increased ( vascular permeability still not increased yet).yet).

Liberation of Histamine like substances Liberation of Histamine like substances acting directly on vessel wallacting directly on vessel wall

INCREASED VASCULAR PERMEABILITY INCREASED VASCULAR PERMEABILITY (LEAKINESS).(LEAKINESS).

Gaps appear between endothelial cells.

Transudate gives way to exudate( protein rich) .

Increases interstitial osmotic pressure contributing to edema

LEUKOCYTE CELLULAR EVENTSLEUKOCYTE CELLULAR EVENTS

Margination and Margination and RollingRolling

Adhesion and Adhesion and TransmigratonTransmigraton

Migration into Migration into Interstitial TissueInterstitial Tissue

TISSUE EVENTSTISSUE EVENTS

Neutrophils and Neutrophils and macrophages in the macrophages in the tissues recognise, tissues recognise, engulf, internalise and engulf, internalise and enzymatically destroy enzymatically destroy micro-organisms or micro-organisms or other foreign other foreign materials as well as materials as well as host cells. host cells.

Phagocytosis

Definition: Is the uptake of particulate material by engulfment.

1. Recognition and attachment of the phagocytic cell to the microbe. 2. Engulfment of the particulate antigen. 3. Killing and degradation of the ingested particle by enzymes and oxygen dependent mechanisms.

TERMINATION OF INFLAMMATIONTERMINATION OF INFLAMMATION

Inflammatory changes may cause tissue Inflammatory changes may cause tissue damage so a tight control is needed. damage so a tight control is needed.

Mediators of inflammation have short half Mediators of inflammation have short half lives .lives .

Stop signals, shift from pro inflammatory to Stop signals, shift from pro inflammatory to anti inflammatory signals.anti inflammatory signals.

CHEMICALCHEMICAL MEDIATORSMEDIATORS

These play an important role in mediating inflammation.These play an important role in mediating inflammation.

They are widely distributed in the body in inactive form.They are widely distributed in the body in inactive form.

Mediators originate either from plasma or from cells.Mediators originate either from plasma or from cells.

Production is triggered by microbial products or by host Production is triggered by microbial products or by host proteins e.g complement / coagulation proteins or kinins.proteins e.g complement / coagulation proteins or kinins.

One mediator triggers the release of other mediator.One mediator triggers the release of other mediator.

Short lived. Inactivation occurs rapidly after release, which Short lived. Inactivation occurs rapidly after release, which is important for control and localization of inflammationis important for control and localization of inflammation. .

Histamine and serotonin-----Histamine and serotonin-----V.D and early increase in V.PV.D and early increase in V.PProstaglandins-------Prostaglandins-------Increased V.P, activate complementIncreased V.P, activate complementNitric oxide------------Nitric oxide------------V.DV.DProstaglandins E2 and I2---Prostaglandins E2 and I2---V.DV.DThrombaxane A2----Thrombaxane A2----Vasoconstriction.Vasoconstriction.Leukotrines--------- Leukotrines--------- Neutrophil chemotaxis, vasoconstriction Neutrophil chemotaxis, vasoconstriction

and increased V.Pand increased V.P

OUTCOMES OF ACUTE INFLAMMATIONOUTCOMES OF ACUTE INFLAMMATION

ResolutionResolution: Acute inflammation usually : Acute inflammation usually disappears after a few days and tissue disappears after a few days and tissue returns to normal.returns to normal.

Progression to chronic inflammationProgression to chronic inflammation: As a : As a result of persistent inflammatory stimuli the result of persistent inflammatory stimuli the inflammatory process can move into a inflammatory process can move into a chronic phase.chronic phase.

Scarring and fibrosis:Scarring and fibrosis:

Inflammation OutcomeInflammation OutcomeChronic

Inflammation

Abscess

Ulcer

Acute

InflammationInjury

Resolution

Abscess Ulcer

Scar

Edema:Edema: Excess of fluid in the interstitial or serous cavities. Excess of fluid in the interstitial or serous cavities. Either transudate or exudate.Either transudate or exudate.

ExudateExudate: Inflammatory extravascular fluid, high protein : Inflammatory extravascular fluid, high protein concentration, cellular debris, specific gravity above 1.020.concentration, cellular debris, specific gravity above 1.020.

TransudateTransudate: Ultra filtrate of plasma. Low protein content : Ultra filtrate of plasma. Low protein content mostly albumin, specific gravity of less than 1.012. mostly albumin, specific gravity of less than 1.012.

Pus:Pus: Purulent exudate, is an inflammatory exudate rich in Purulent exudate, is an inflammatory exudate rich in leukocytes, dead cell debris and microbes.leukocytes, dead cell debris and microbes.

Morphologic Patterns 1- Serous InflammationMarked by a thin fluid that derived from blood serum or mesothelial cells2- Fibrinous InflammationA fibrinous exudate develops with large vascular leakCharacteristic of inflammation in body cavities (pericardium , pleura and meninges)3- Suppurative or Purulent InflammationCharacterized by large amounts of purulent exudate (pus) Pus consists of neutrophils, necrotic cells, and edema 4- UlcersA local defect or excavation of the surface of epithelial covering.

Serous inflammation Fibrinous Inflammation

Suppurative inflammation