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DR EJAZ WARIS Inflammation"Opportunities are usually disguised by hard work, so most people don't recognize them." - Ann Landers

Inflamation

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Page 1: Inflamation

DR EJAZ WARIS

Inflammation-1

"Opportunities are usually

disguised by hard work, so

most people don't recognize

them."

- Ann Landers

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Shashi-Mar 2000

Inflammation-2

INFLAMMATI0N

Dr. SHAHILA JALEEL

Histopathology

SZH,Lahore

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Introduction:

“Inflame” – to set fire.

Inflammation is “dynamic response of vascularised tissue to injury.”

Is a protective response.

Serves to bring defense & healing mechanisms to the site of injury.

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INTROD……….

Injurious stimuli cause a protective vascular connective tissue reaction called “inflammation”• Dilute

• Destroy

• Isolate

• Initiate repair

Acute and chronic forms

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Lewis Triple Response:

Flush: capillary dilatation.

Flare: arteriolar dilatation.

Weal: exudation, edema.

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Gastric Ulcer:

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Laryngitis:

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Acute Enteritis:

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Pneumonia

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Cardinal Signs of Inflammation

Rubor : Redness – Hyperaemia.

Calor : Warm – Hyperaemia.

Dolor : Pain – Nerve, Chemical med.

Tumor: Swelling – Exudation

Loss of Function:

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Heat Redness Swelling Pain Loss Of Func.

The 5 Cardinal Signs of

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Inflammation

Two main components:

vascular reaction

cellular reaction

Two main types:

acute

chronic

Chemical mediators

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Cells of inflammation

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Circulating cells

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Connective tissue matrix

Made up of :

A)collagen fibers

B)elastic fibers

C)glycoproteins

D)proteoglycans

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Connective tissue cells

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Acute Inflammation - Mechanism

1.Alterations in

vascular calibre

leading to

increased blood

flow

2.Microvasculature

structural changes

3.Leukocyte

emigration

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Vascular changes

A Inconstant transient vasoconstriction of arterioles for few seconds followed by vasodilation

Accounts for warmth and redness

Opens microvascular beds

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

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Vascular permeability (leakiness) commences

Transudate gives way to exudate(protein-rich)

Increases interstitial osmotic pressure contributing to edema (water and ions)

slowing of circulation (increased permeability of the vasculature)

stasis

Leukocyte migration

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Vascular changes continued

B)increased vascular permeability

vascular leakage leading to escape of protein rich fluid into the interstitium is the hall mark of acute inflammation

exudate

transudate

edema

pus

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An exudate is an extravascular fluid that has a

high protein concentration

cellular debris

high specific gravity.

Its presence implies an increase in the normal permeability of small blood vessels in an area of

injury .

A transudate is a fluid with

low protein content (most of which is albumin)

little or no cellular material

low specific gravity

It is essentially an ultrafiltrate of blood plasma that results from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability

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Edema denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate.

Pus, a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils), the debris of dead cells and, in many cases, microbes.

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IMMEDIATE TRANSIENT RESPONSE – RESPONSE

TO

MINOR INJURY

IMMEDIATE SUSTAINED RESPONSE – RESPONSE

TO

MORE SERIOUS INJURY, CONTINUES FOR

SEVERAL

DAYS, DAMAGE TO VESSELS

DELAYED RESPONSE – INCREASES IN CAPILLARY

PERMEABILITY, DELAYED 4-24 HR, RADIATION

INJURIES, SUNBURN

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Inflammation-37How does endothelium becomes

leaky in inflammation?

1)formation of endothelial gaps in venules

2)cytoskeletal reorganization

3)increased transcytosis

4)direct endothelial injury

5)leukocyte dependent injury

6)delayed prolonged leakage

7)leakage from new blood vessels

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Mechanism of Inflammation:

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Leukocyte emigration/extravasation

Sequence of events in the journey of leukocytes from the lumen to the interstitial tissue

Margination

Pavementing

Rolling

Adhesion

Transmigration/diapedesis

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Adhesion molecules

Play an important role in acute inflammation

4 families

Family no 1: Selectins

E-selectin,P-selectin,L-selectin

Family no 2:Ig-family adhesion proteins

ICAM-I,ICAM-II,PECAM-I,VCAM-I

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Adhesion molecules

Family no 3:Integrins

LFA

MAC-1

VLA-4

Family no 4:Mucin like glycoproteins

CD-34

Glycam-1

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Neutrophil Margination

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Vascular changes

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Pneumonia - Exudation

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"Each time you are honest and conduct

yourself with honesty, a success force will

drive you toward greater success. Each

time you lie, even with a little white lie,

there are strong forces pushing you

toward failure."