Inflammation is the local response of tissues to infection, injury, or antigen-antibody reaction. The signs are rubor, tumor, calor, dolor, and functio laesa. Acute inflammation is characterized by fluid and plasma accumulation, neutrophil infiltration, and exudation of leukocytes. Vascular events include vasodilation, increased permeability and leukocyte margination. Cellular events involve leukocyte adhesion, emigration, chemotaxis, phagocytosis, and secretion of inflammatory mediators. Chronic inflammation is longer-lasting and features mononuclear cell infiltration and tissue destruction. Granulomatous inflammation forms aggregates of epithelioid macrophages surrounding foreign bodies or inducing immune responses. Systemic

1. INFLAMMATION
G.M.Kailash kumar
First year Pg

2. DEFINITION
local response of vascularized
tissues to infection / injury due to
any agent that brings cells and
molecules of host defense from
circulation to site where they are
needed , in order to eliminate the
offending agents.

3. AGENTS
 Physical
o Heat
o Cold
o Radiation
o Trauma
 Chemical
 Organic and inorganic poison
 Infective
 Bacteria virus & their toxin
 Immunological agent
 Cell mediated and antigen –antibody reaction

4. SIGNS
Rubor
Tumor
Calor
Dolar
Functio laesa- virchow

5. TYPES
Acute
Chronic
Subacute

6. ACUTE INFLAMMATION
Short duration - early response - repair
Features
 Fluid and plasma accumulation
 Intravascular platelet activation
 Neutrophils
 Fluminant acute inflammation

7. Vascular
events
Haemodynamic
changes
Altered
vascular
permeability
Cellular
events
Exudation of
leucocyte
phagocytosis

8. HAEMODYNAMIC CHANGES
 Transient vasoconstriction
 Arterioles
 progressive vasodilation
 Mainly arterioles
 With in half an hour of injury
 Responsible for redness and warmth
 ↑ed local hydrostatic pressure
 Transudation - swelling
 Stasis
 Increased permeabilty - increased RBCs
 Leucocytic margination
 Mainly neutrophils

9. LEWIS EXPERIMENT
Red line
Flare
Wheal

10. ALTERED VASCULAR PERMEABILITY
 Contraction of endothelial cells
 Most common mechanism
 Venules
 Histamin & bradykinin
 Reversible ,short duration (15-30 min)
 Retraction of endothelial cells
 Reversible retraction of intercellular junction
 Venules
 IL-1 , TNF
 4-6 hrs to 24 hrs

11.  Direct injury to endothelial cells
 Injury – cell necrosis
 All microvasculature
 Immediate sustained leakage – bacterial infection
 Delayed prolonged leakage – thermal & radiation injury
 Endothelial injury mediated by leucocytes
 Activation of leucocytes – proteolytic enzyme- endothelial
injury – leakiness
 Late response
 Other mechanisms
 Neovascularization

12. CELLULAR EVENTS
 Exudation of leucocytes
 Changes in the formed element of the blood
vasodilatation
Increased
blood flow
Stasis
Altered
axial flow
of blood
Exudation Margination

13.  Adhesion /rolling
 Selectin ( P,E,L)
 Addressins
 Integrins (β1,β2)
 Immunoglobulin superfamily
adhesion molecule (ICAM-1,2)

14. Emigration
Collagenase
Emigration
 Diapedesis
- emigration of RBCs
Chemotaxsis
 LTB4
 PF4
 C5a
 IL-8
 MCP-1
 CD4+ T Cells
 Leucocyte activation
 Production of arachidonic acid
metabolite
 Degranulation & secretion of
lysosomal enzyme
 Generation of o2 metabolite
 Increased intracellular calcium
 Increased leucocyte surface
adhesion molecule

15. PHAGOCYTOSIS

16. PHAGOCYTOSIS
 Types
 Microphages
 Macrophage
 Steps
 Attachment stage
 Engulfment stage
 Secretion stage
 Killing or degradation stage
 Oxygen dependant
 Oxygen independent
 Nitric oxide mechanism

17. o Attachment stage
o Opsonins
 Ig G opsonins
 C3b opsonins
 Lectins
o Engulfment stage
o Formation of cytoplasmic pseudopods
o Phagosomes + lysosomes = phagolysosomes

18. SECRETION / GEGRANULATION
 Discharge of stored granule into phagosomes
 Synthesis & secrete IL 2 & 6, TNF
 Archidonic acid metabolite ( Pg , IL, PAF)
 Oxygen metabolite ( o’2 , H2 O2 , HOCL )

19. KILLING / DEGRADATION
 Killed by antibacterial
 Degraded by hydrolytic enzyme
 Three mechanism
 Oxygen depentant
 Oxygen indepentant
 Nitric oxide

20. OXYGEN DEPENTANT
2O2 + NADPH -------------------- 2O’2 + NADP+ + H+
NADPH oxidase
O’2 + 2H+ ---------------------------- H2O2
MPO
H2O2 ---------------------→HOCL + H2O2
Cl’,Br’,I’

21. CHEMICAL MEDIATORS OF INFLAMMATION
 Cell derived mediators
 Vasoactive amines
 Arachidonic acid metabolite
 Lysosomal component
 Platelet activating factor
 Cytokines
 Nitric oxide and oxygen metabolite
 Plasma derived mediators
 Kinin system
 Clotting system
 Fibrinolytic system
 The complement system

22. Oxygen independent
Lysosomal hydrolase, permeability increasing factors,
defensin, cationic protein
Nitric oxide mechanism
from endothelial cell and activated macrophages
fungicidal & antiparasitic action

27. LYSOSOMAL COMPONENT
 Granules of neutrophils
 2’ - Lactoferrin , lysozyme, alkaline phosphatase,
collagenase, proteinase.
 1’ - myeloperoxidase, acid hydrolase , elastase ,
collagenase, proteinase
 Granules of monocyte and tissue macrophages
 Protease,collagenase, elastase and plasminogen
activators

28. PAF
 Released from IgE sensitized basophil or mast cell
 Increased vascular permeability
 Vasodilation in low concentration
 Vasoconstriction
 Bronchoconstriction
 Adhesion of leucocyte to endothelium
 chemotaxis

29. CYTOKINES
 Polypeptide substance from lymphokines and
monokines
 IL-1
 TNF ,β
 IF -γ
 IL-8,PF-4

30. NITRIC OXIDE AND OXYGEN METABOLITE
 vasodilation
 Antiplatelet activating agent
 Possibly microbial action
 Endothelial cell damage - ↑vascular permeability
 Avtivation of protease , inactivation of anti-protease
– tissue matrix damage
 Damage to other cell

31. PLASMA DERIVED MEDEATORS
 The kinin system
 The clotting system
 The fibrinolytic system
 The complement system

32. THE KININ SYSTEM
Factor XII
Factor XII a
prekallikerin activator
Plasma prekalikerin kallikerin
kininogen BRADYKININ

33. THE CLOTTING SYSTEM
Factor XII XIIa
XI XIa
+
VIIIa
+
PF3
X Xa
+
Va
+
PF3
prothrombin thrombin
Fibrinogen Fibrin
plasmin
Fibrinopeptide

34. THE FIBRINOLYTIC SYSTEM
Plasminogen activator
(kallikerin,XIIa,Leucocyte,endothelium)
Plasminogen plasmin
plasmin
C3 C3a Fibrin split product

35. THE COMPLEMENT SYSTEM
I. Antigen –antibody complex
II. Non immunologic agent – bacterial toxin, cobra venom
and IgA
Anaphylotoxin:
- Realese of histamin from mast cell and basophils
- Increased vascular permeability – oedema
 C3a – augment phagocytosis
 C5a – chemotactic for leucocyte
 C4a
 Membrane attack complex (MAC) - cause pore in cell
membrane for the invading micro organism

36. INFLAMMATORY CELLS
 PMN
 Eosinophils
 Basophils
 Lymphocyte
 Plasma cells
 Mononuclear phagocyte system
 Giant cells

39. GIANT CELLS

40. DETERMINING FACTORS
 Factors involving the organism
 Type of injury, virulence, does,
product of organism,entry
 Factors involving the host
 General health, immune state, leukopenia, site,local
host factor
 Type of exudation
 Serous, fibrinous, purulent,haemorrhagic,catarrhal
 Cellular proliferation
 Necrosis

41. EFFECTS OF INFLAMMATION
 Fever
 Leucocytosis
 Lymphangitis
 shock

42. FATE OF INFLAMMATION
 Resolution
 Healing
 To suppuration
 Chronic inflammation

43. FATE OF INFLAMMATION
 Resolution
 Healing by scarring
 Progression to suppuration
 Progression to chronic inflammation

44. CHRONIC INFLAMMATION
 Is of longer duration and occurs either after the
causative agents of acute inflammation persist for a
long time, or the stimuli
 3 ways
 Following acute inflammation
 Recurrent attack
 Starting as de nova

45. FEATURES
Mononuclear cell
infiltration
Tissue destruction or
necrosis
Proliferative changes

46. TYPES
Non
specific
Specific

47. SYSTEMIC EFFECT
 Fever
 Anaemia
 Leucocytosis
 ESR
 Amyloidosis

48.  Is a distinctive pattern of inflammation
characterized by aggregates of activated
macrophages that assume an epithelioid
appearance.
 A granuloma is a focus of chronic inflammation
consisting of microscopic aggregation of
macrophages that are transformed in to epithelium
like cells.
GRANULOMATOUS INFLAMMATION

52. TYPES OF GRANULOMA
Foreign body granuloma
Immune granulomas

53.  Foreign body granulomas form around material
such as talc, sutures or other fibers.
 They do not incite any specific inflammatory or
immune response.
FOREIGN BODY GRANULOMA

54. IMMUNE GRANULOMA
 Caused by variety of agents that are capable of
inducing a cell mediated response.

55. SYSTEMIC EFFECT OF INFLAMMATION
 Fever
 Leukocytosis
 Increased pulse and blood pressure
 Decreased sweating
 Rigors
 Chills
 Malaise

56. Thank you