The document discusses inflammation, including its causes, types, components, and mechanisms. It describes the vascular and cellular components of acute inflammation. The vascular component involves vasodilation, increased permeability and exudation. The cellular component involves the emigration of white blood cells from blood vessels to tissue through a process of margination, rolling, tight adhesion, and diapedesis. Together these components work to destroy pathogens and initiate healing through removal of dead cells and debris.

1. Kamal Ch. Upreti
Pharmaceutical marketing
INFLAMMATION

2. INFLAMMATION
GOOD SIDE BAD SIDE

3. INFLAMMATION
“A dynamic response of vascularised tissue to injury.”
Host ImmunityHost Immunity

4. INFLAMMATION
Causes of inflammation
Physical
Chemical
Mechanical
Thermal
Biological

5. TYPES OF INFLAMMATION
ACUTE
INFLAMMATION
CHRONIC
INFLAMMATION
Rapid Development &
Short life
Slow Development
& Last will long

6. ACUTE INFLAMMATION
Non-specific response to any cell injury
Involves blood vessels, chemical mediators, and
white blood cells
Purposes
Destroy an organism
Limit damage to a certain area
Prevent reproduction of an organism Virus, bacterium
Clear debris and lay groundwork for healing

7. Heat Redness Swelling Pain Loss Of Func.
The 5 Cardinal Signs of
ACUTE INFLAMMATION

8. Inflammation is characterized by five cardinal signs:-
Rubor (redness),
Calor (increased heat),
Tumor (swelling),
Dolor (pain), and
Functio laesa (loss of function).
Cardinal Signs (primary or major clinical sign)

9. Vascular component Cellular component
Two components
ACUTE INFLAMMATION
Arteriolodilation Microcirculation
EXUDATION

10. Inflammation - Mechanism
1. Vasodilatation
2. Exudation - Edema
3.
4. Emigration of cells
5. Chemotaxis
Vascular component
Cellular component

11. Vascular Events
Initial vasoconstriction near site of injury
Vasodilation of arterioles and capillaries
Increased blood flow to the area
Increased hydrostatic pressure

12. Vascular Events
HISTAMIN
PROSTAGLANDINS
NITRIC OXIDE
BRADIKININ
PARANCHYMAL CELL

13. NORMAL BLOOD FLOW
Hydrostatic Pressure
Osmotic Pressure
Vascular Events

14. DURING INJURY
PLASMA
PROTEIN
LEAKOUT
Hydrostatic Pressure
Osmotic Pressure
Vascular Events

15. HISTAMIN
PROSTAGLANDINS
NITRIC OXIDE
ENDOTHELIAL CELL
Vascular Events

16. Vascular Events
Increased capillary permeability
Secondary to tight junction disruption in endothelial
layer of blood vessels
Plasma moves out of the blood vessels (exudate)
Exudate = large amount of protein
Transudate = relatively little protein

17. ENDOTHELIAL
CELL
HISTAMIN
PROSTAGLANDINS
NITRIC OXIDE
TNF
CYTOKINES
THROUGH GENOMIC
PROGRAMME OF PR-CEL
CONTRECTION
Short Time
RETRECTION
Long Time
NORMAL
CELL
Vascular Events

18. Fluid environment surrounding inflammation is thick
with cells and debris
Cells and debris will become purulent over time
Vascular Events

19. Rubor, Calor, Tumor
Vascular Events

20. Kinin cascade
Group of plasma proteins that stimulate the
vascular component of inflammation
Bradykinin is most important kinin
Kinins and prostaglandin E cause pain at site
Chemical Mediator

21. Histamine Stimulates vascular component of inflammation
Nitrous oxide -Promotes vasodilation , Blocks platelet clumping
and clot formation , Cytotoxic.
Aracodonic acid metabolites from cell membrane phospholipids
Leukotrienes (C-4, D-4, E-4) maintain inflammation in cellular and
vascular inflammation
Prostaglandins prolong inflammatory process
PGD2, E2, F2 - Vasodilation and increased capillary permeability
PGI2 – vasodilation, inhibits platelet clumping
Chemical Mediator

22. Vascular component Cellular component
Two components
Microcirculation
EXUDATION
Arteriolodilation
WBCs
Chemotaxis
Emigration of cells

23. Cellular component
How WBC pass through Vascular component to Interstitial component ?

24. Cellular Components of Inflammation
Primary circulating WBC's are granulocytes
1.) Neutrophils
2.) Eosinophils
3.) Basophils
Other components:
platelets, monocytes (precursors of macrophages),
and lymphocyte-like natural killer cells (NK cells)

25. Neutrophils and monocytes (phagocytes)
move to the inflammatory site
Margination
Phagocytes adhere to the blood vessel walls

26. Emigration (diapedesis)
Phagocytes slip out of the blood vessels through
endothelial junctions
Neutrophils arrive the earliest – 6-24 hours
Monocytes arrive approx. 24-48 hours after injury

27. Phagocytosis
WBC recognizes and attaches to the organism or
antigen
The organism is engulfed
Degranulation (release of lysosomes) leads to death
of the organism
Platelet clumping at the site of injury

28. Cellular Events
Emigration of Leukocytes
from Vascular components to cellular components
Chemotaxis
Leukocyte movement towards the source of
Inflammation

29. How the WBC pass the vascular
compartment to Interstitial Components ?

30. Emigration of Leukocytes

31. M
argination
R
olling
Tight
Adhesion
Imigration
Diapediasis

32. Normal Blood Flow

33. Vascular Events
Hydrostatic PressureHydrostatic Pressure
Protein Rich Fluid -ExudationProtein Rich Fluid -Exudation
More Viscus BloodMore Viscus Blood
Less blood velocityLess blood velocity
Coming blood increaseComing blood increase
Normal Blood Flow- DisturbedNormal Blood Flow- Disturbed

34. RBC start sticking to each other
Protein rich fluid - Exudation Increase Blood viscosity

35. 1- Margination
WBC now hit the endothelial cell

36. Chemical Mediator act on the endothelial cell— Activation
The sticky molecule of WBC –SIALATED SUGAR (oligisaccharide)
Adhesion of WBC with Endothelial cell
But the conjugation is not longer

37. 2- ROLLING
Sticky WBC rolling with Endothelial cell

38. 3- Tight Adhesion
Chemokines released from inflammatory area, attached with
Endothelial cell surface- IL8- Induced

39. Activated
INTEGRINE (peptide)
Non
activated
INTEGRINE
Chemomkines
ICAM-
Inter Cellular
Adhesion Molecule
VCAM-
Vascluar Cellular
Adhesion Molecule
Chemokine stimulate the INTEGRINE and this INTEGRINE bind with
ICAM, VCAM
Strong Bonding of WBC with Endothelial cell -Tight adhesion

40. 4- DIAPEDIASIS (Imigration, Extravassation, Migration )
PECAM-
Platelet Cell Adhesion Molecule
Homophilic Interaction
Collegenase -Make a hole on endothelial lining

42. Gprotein C-Receptor - IP3-ER-Activation – Proteinkinase-C - Polymer
Chemoattractant
Chemotaxis

44. Systemic effects of inflammation
● Fever
● Effects of pyrogen from neutrophils and
macrophages
● Effects of interleukin-1 on hypothalamus
●Increased temp is harmful to some organisms (good)
●Some organisms release endotoxins when
killed(bad)

45. Leukocytosis
● Stimulated by complement (C3a)
● Large release of stored neutrophils
● Production of leukocytes by bone marrow
Loss of appetite
Increased deep sleep
Weight loss
Weakness
Systemic effects of inflammation

46. Benefits of Inflammation
1.) CONTROLS TISSUE DAMAGE
●The clotting systems and WBC's (i.e.
eosinophils)

47. 2.) PREVENTS INFECTION
The plasma protein systems that help destroy
and contain bacteria (i.e. complement &
clotting systems) and the influx of WBC's
Benefits of Inflammation

48. 3.) INITIATES THE ADAPTIVE IMMUNE
RESPONSE
4.)INITIATES HEALING THRU REMOVAL OF
DEAD CELLS
Benefits of Inflammation

49. Return to normal vascular permeability
Removal of edema and plasma proteins by
lymphatics and macrophages
Phagocytosis by macrophages
Cellular debris and dead neutrophils removed
Resolution of inflammation

51. THANK YOU