Inflamation
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Transcript of Inflamation
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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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DR EJAZ WARIS
Inflammation-8
Laryngitis:
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Acute Enteritis:
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DR EJAZ WARIS
Inflammation-10
Pneumonia
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DR EJAZ WARIS
Inflammation-11
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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DR EJAZ WARIS
Inflammation-13
Inflammation
Two main components:
vascular reaction
cellular reaction
Two main types:
acute
chronic
Chemical mediators
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DR EJAZ WARIS
Inflammation-14
Cells of inflammation
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Circulating cells
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DR EJAZ WARIS
Inflammation-16
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DR EJAZ WARIS
Inflammation-17
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DR EJAZ WARIS
Inflammation-18
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DR EJAZ WARIS
Inflammation-19
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DR EJAZ WARIS
Inflammation-20
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DR EJAZ WARIS
Inflammation-21
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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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DR EJAZ WARIS
Inflammation-24
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DR EJAZ WARIS
Inflammation-25
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DR EJAZ WARIS
Inflammation-26
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DR EJAZ WARIS
Inflammation-28
Acute Inflammation - Mechanism
1.Alterations in
vascular calibre
leading to
increased blood
flow
2.Microvasculature
structural changes
3.Leukocyte
emigration
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DR EJAZ WARIS
Inflammation-29
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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DR EJAZ WARIS
Inflammation-31
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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DR EJAZ WARIS
Inflammation-33
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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DR EJAZ WARIS
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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DR EJAZ WARIS
Inflammation-39
Mechanism of Inflammation:
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DR EJAZ WARIS
Inflammation-40
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DR EJAZ WARIS
Inflammation-41
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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DR EJAZ WARIS
Inflammation-45
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DR EJAZ WARIS
Inflammation-46
Neutrophil Margination
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DR EJAZ WARIS
Inflammation-47
Vascular changes
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DR EJAZ WARIS
Inflammation-48
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."