acute inflammation.pptnz. I. D. Id. Ie. I ecie cinxie. India neicb

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1. INFLAMMATION
Dr.Kamini Patel
Dept of pathology
GMERS medical college
valsad

2. “Inflame”–tosetfire.
Inflammationis“Adynamicresponseof
vascularisedtissuetoinjury.”
Itisaprotectiveresponse.
Itservestobringdefense&healing
mechanismstothesiteofinjury.

3. Acute inflammation
Chronic inflammation
RepairResolution
Abscess
Injury

4. Etiologies
Physical agents : heat,cold,radiation,mechanical
trauma.
Chemical agents : organic and inorganic poisons.
Infective agents : bacteria,viruses and their toxins.
Immunological agents : cell mediated immunity and
antigen-antibody reactions.

5. SIGNS of inflammation
4 cardinal signs of inflammation as
described by Celsusin 1
st
century A.D.:
Rubor -Redness
Tumor -Swelling
Calor -Heat
Dolor -Pain
Virchowadded a fifth sign
Functio laesa-Loss of function

6. CARDINAL SIGNS OF ACUTE INFLAMMATION
Heat Redness Swelling Pain Loss of function
Celsius (30 BC) Virchow (1902)

7. TYPES of Inflammation
I) Acute inflammation
Short duration (Less than 48 hours)
Cell involved is Polymorphonuclear leukocyte (PMN)
II) Chronic inflammation
Long duration (Greater than 48 hours (weeks,
months, years))
Cells involved are Mononuclear cells (Macrophages,
Lymphocytes, Plasma cells)

8. Acute inflammation
Chronic inflammation
RepairResolution
Abscess
Injury

9. Acute inflammation:
DEFINATION :
Changes which take place usually within the first
few minutes to several hours to days after an injury
Most commonly involves PMN’s as mediators

10. PATHOGENESIS:THREEmainprocessesoccuratthe
siteofinflammation,duetothereleaseofchemical
mediators:
I)VACULAREVENTS:
1.Changesinvascularflowandcaliber
(hemodynamicchanges)(rednessandwarmth).
2.Changesinvascularpermeability(vascular
leakage)(swelling,pain&lossoffunction).
II)CELLULAREVENTS:
3.LeukocyticInfiltrationandphagocytosis.

12. 1.Changes in vascular flow and caliber
(hemodynamic changes)
1)Vasoconstriction
2)Vasodilatation
3)Local hydrostatic pressure
4)Slowing of the circulation
5)Leukocyte margination

13. 1.Changes in vascular flow and caliber
(hemodynamic changes)
1)Vasoconstriction
-transient (3-5sec.)and inconstant
-Involves arterioles
2) Vasodilatation
-within half an hour of injury
-Involves first the arterioles, then venulesand
capillaries
-Result in increased blood volume in microvascular
bed of the area
-Responsible for redness and warmth

14. 1.Changes in vascular flow and caliber
(hemodynamic changes)
(3)Local hydrostatic pressure
-elevate pressure resulting in transudation of fluid in
extracellular space
-responsible for swelling
(4)Slowing or stasis of the circulation
outpouring of albumin rich fluid into the extravascular
tissues results in the concentration of RBCs in small
vessels and increased viscosity of blood.
(5)Leukocyte margination
Leukocytes(PMNs) become oriented at the periphery of
vessels and start to stick

16. Lewis Triple Response
Haemodynemic changesin
inflammation is best demonstrated
by lewis experiment (sir thomas
lewis) in 1924.
Lewistripleresponseisthe
characteristic3partresponsethat
developswhenalineismadebya
strokingontheskin.Itisproduced
duetothereleaseofhistaminefrom
themastcells.

17. Components of the Triple Response
1.Red line:appears in few seconds, transient local
vasodilation(capillaries, venules)
2.Flare : appears in 20-30 seconds,flush
surrounding the red line,vasodilation(arterioles)
3.wheal: appear in few minutes,swelling or oedema
of the surrounding skin due to transudation of
fluid into the extravascular space.

19. 2.Changes in vascular permeability
(vascular leakage)
Starling's hypothesis
In normal tissue from arteriole to venule:
Intravascular
hydrostatic
pressure
@
Colloid
osmotic
pressure

20. 2.Changes in vascular permeability
(vascular leakage)
In inflammation from arteriole
to venule:
Intravascular
hydrostatic
pressure
Colloid
osmotic
pressure
+ = Edema

22. In the initial stage of inflammation
Escape of fluid is due to vasodilatation
And consequent elevation of hydrostatic prassure
This is transudatein nature
Consequently increased vascular permeability of
microcirculation
This is exudatein nature

23. DIFFERANCE
TRANSUDATE EXUDATE
An ultrafiltrate of blood
plasma
permeability of
endothelium is usually
normal.
low protein content (
mostly albumin)
specific gravity less than
1.012
Few cells
A filtrate of blood plasma
mixed with inflammatory
and cellular debris.
permeability of
endothelium is usually
altered
high protein content
specific gravity greater
than 1.020
Many cells

24. 2.Changes in vascular permeability
(vascular leakage) (cont)
MECHANISMS :
Contraction of endothelial cells
Direct injury to endothellial cells
leukocyte-dependent injury
Increased transcytosis
New blood vessels formation

26. CELLULAR EVENTS
3.Leukocyte exudation and phagocytosis
Escape of leukocytes from the lumen
of microvasculature to the
interstitial tissue called….

27. Leukocyte exudation
divided into 3 steps
1. Margination and rolling
2. Adhesion and Diapedesis
(transmigration across the endothelium)
3. Migration toward a chemotactic
Stimulus(chemotaxis)

28. Leukocyte exudation
1 )Marginationand Rolling:
WBC slow down and are pushed to the side of the
vessel near endothelial cells. This process is
“Margination”
WBC’s transiently stick to endothelial cells. This
process is “Rolling”

29. Leukocyte exudation
2. Adhesion and Transmigration:
The adhesion is facilitated by the action of
adhesion molecules called “Selectins”.
Selectinsare present on WBC, endothelial cells
and platelets.
E-Selectin: on endothelial cell
P-Selectin: on Platelets and endothelial cells
L-Selectin: on WBC’s
Selectinsare up regulated by IL-1, and TNF.

30. Leukocyte exudation
Other adhesion molecules are :
Integrins
ICAM (intercellular adhesion molecule)
VCAM (vascular adhesion molecule)
Mucin like glycoproteins.
Transmigration occurs as the WBC’s pass through
intercellular junction. This process is facilitated by
PECAM (platelet endothelial cell adhesion molecule,
CD31).

31. Leukocyte exudation
3. Migration in interstitium: Chemotaxis
Migration of WBC’s after crossing several
barriers(endothelium,basementmembrane,matrix)to
reach the interstitial tissue called is Chemotaxis
facilitated by chemotactic agents. These are molecules
that attract WBC’s.
They include:
a.Bacterial products
b.Complement system, C5a
c.Leukotriene B4 (LTB4)
d.Cytokines (IL-8)

33. Leukocytic Margination
and Sticking
Phagocytosis
Chemotaxis

34. Tissue oedemaNeutrophil margination …. And emigration

35. phagocytosis
DEFINATION:
Process of engulfment of solid particulate material to
the cells (cell eating).
Twomain type of phagocytic cells :
1)Polymorphnuclearneutrophil (PMNs)
2)Circulating monocytes(macrophage)

36. PROCESS(3 STEPS)
1. Recognition and attachment:
“opsonins”:
-immunoglobulins IgG
-C3b molecule of the complement system
Collectins
WBC’s have specific receptors to these opsonins.

37. Phagocytosis
2. Engulfment in phagocytic vacuole:
phagosome.
3. Killing and degradation:
Phagosome fuses to lysosome to form
phagolysosome.
Killing is facilitated by:
a.Oxygen free radicals (oxidative burst)
b.Lysosomal enzymes (myeloperoxidase)

38. 2 MECHANISMS
Oxygen dependent
Myeloperoxidase dependent
(the most important!)
Myeloperoxidase independent
Oxygen independent

39. Process of Phagocytosis

40. Acute Enteritis:

43. Outcome of Acute Inflammation:
1.Resolution
2.Abscess formation
3.Progression to chronic inflammation
4.Scarring and Fibrosis
organization and fibrosis

45. Abscess formation:
"A circumscribed collection of pus appearing in
an acute or chronic localized infection, and
associated with tissue destruction, and
frequently, swelling.“
It is usually the result of a pyogenic organism.