12/14/2011

1. Inflammation-1
"Opportunities are usually
disguised by hard work, so
most people don't recognize
them."
- Ann Landers
DR EJAZ WARIS

2. Inflammation-2
INFLAMMATI0N
Dr. SHAHILA JALEEL
Histopathology
SZH,Lahore
Shashi-Mar 2000

3. 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.

4. INTROD……….
 Injurious stimuli cause a protective
vascular connective tissue reaction
called “inflammation”
• Dilute
• Destroy
• Isolate
• Initiate repair
 Acute and chronic forms

6. Lewis Triple Response:
 Flush: capillary dilatation.
 Flare: arteriolar dilatation.
 Weal: exudation, edema.

7. Gastric Ulcer:

8. Inflammation-8
Laryngitis:
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9. Acute Enteritis:

10. Inflammation-10
Pneumonia
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11. 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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12. The 5 Cardinal Signs of
Heat Redness Swelling Pain Loss Of Func.

13. Inflammation-13
Inflammation
Two main components:
vascular reaction
cellular reaction
Two main types:
acute
chronic
Chemical mediators
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14. Inflammation-14
Cells of inflammation
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15. Circulating cells

16. Inflammation-16
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17. Inflammation-17
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18. Inflammation-18
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19. Inflammation-19
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20. Inflammation-20
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21. Inflammation-21
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22. Connective tissue matrix
 Made up of :
 A)collagen fibers
 B)elastic fibers
 C)glycoproteins
 D)proteoglycans

23. Connective tissue cells

24. Inflammation-24
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26. Inflammation-26
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28. 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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29. 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) DR EJAZ WARIS

30.  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

31. 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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32.  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

33. 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.
DR EJAZ WARIS

36.  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

37. Inflammation-37
How 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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39. Inflammation-39
Mechanism of Inflammation:
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40. Inflammation-40
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41. 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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42. 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

43. Adhesion molecules
Family no 3:Integrins
LFA
MAC-1
VLA-4
Family no 4:Mucin like glycoproteins
CD-34
Glycam-1

45. Inflammation-45
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46. Inflammation-46
Neutrophil Margination
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47. Inflammation-47
Vascular changes
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48. Inflammation-48
Pneumonia - Exudation
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49. "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."