2. INFLAMMATION
Definition – Inflammation is a response of vascularized
connective tissue to infections and damaged tissues that
brings cells and molecules of host defense from the
circulation to the sites where they are needed ,in order to
elimante the offending agents.
It is a protective response that is essential for survival.
Inflammation involve2 basic process -:
1. Early –inflammatory response
2. later -repair
3. CAUSE OF INFLAMMATION
1.INFECTION-
It is most common and medically important causes of
inflammation.
2. TISSUENECROSIS-
Caused by various agents such as –
Ischemia
Physical Agents
Chemical agents
3. IMMUNOLOGICAL AGENTS
Cell mediated
Antigen-antibody reaction
4. INERT MATERIALS
14. Cellular Events;
It includes:
Recruitmentof leucocytes
Activation to recognize the microbe
Phagocytose and clearing of offending agent.
Discussed under-
Exudation of leucocytes
Phagocytosis
15. EXUDATION OF LEUCOCYTES;
1. CHANGES IN THE FLOW OF BLOOD
2. ROLLING AND ADHESION
3. TRANSMIGRATION
4. CHEMOTAXIS
16. CHANGES IN FLOW OF
BLOOD;
VASODIALATATION
SLOWING AND STASIS OF BLOOD
WIDENING OF CENTRAL STREAM OF
CELLS
NARROWING OF CELL
FREE LAYER OF PLASMA
REDISTRIBUTION OF CELLS
18. TRANSMIGRATION;
• MOVEMENT OF NEUTROPHILL
• ALONG ENDOTHELIAL CELLS
• CYTOPLASMIC PSUDOPODS OF
• NEUTROPHILLS
• NEUTROPHILL LODGE B/W ENDOTHELIAL
• CELL AND BASEMENT MEMBRANE
• MONOCYTES AND MACROPHAGES APPEARS
• ESCAPE OF RBC’s
19. Chemotaxis;
Movement of leucocytes toward the direction of
chemical molecules or factors
Chemoattractants are of two
types
Exogenous agents
Endogenous agents
Leucotrienes
Complement system
Cytokines
kallikrein
20. Mechanism of chemotaxis;
binding of
Chemoattractant
Release of
effector
molecules
Increase of
cytosolic calcuim
Cytoskeltal
changes
21. Phagocytosis;
process of cellular engulfment of solid
particles of solid particulate material
Two main type of cells are involved
• Polymorphonuclear neutrophils
• Macrophages
Production of proteolytic enzymes
Steps of phagocytosis
o Recognition and attachment
o Engulfment
o Killing and degradation
22. Recognition and
attachment;
Expression of cell surface
receptors on macrophages
Coating of microorganisms
Opsonisation
o IgG opsonin
o C3b opsonin
o Collectin
30. Properties Of these
mediators
Injurious agents
Dead & damaged tissues
Presence of other mediators
01; Release in response to stimuli.
SECONDARY MEDIATORS
AntagonizeOR Agonize
The action of prior
mediators
31. Cell derived mediators
Synthesized in Liver
Plasma
Protein
derivative
Presynthesized/stored in
granules
Freshly synthesis
within cell
Require
activation
02; release of mediators
32. 03; Their actions on targets
Can act on
differenttargets
Similar actions or
differentactions
On different
targets
1
2
3
33. 04; Range of actions
Chemotaxis
Fever
Pain
Tissuedamage
Increased vascularpermiability
vasodialation
34. 05; Mediators have short life span
Rapidlymetabolized by-
Enzymatic
inactivation
Antioxidants
Regulatory
proteins
Decay
spontaneously
38. Lysosomal components;
• Granules of neutrophils
a) Primarygranules - functionallyactiveenzymes,
b) Secondarygranules –alkalinephosphatase,
c) Tertiarygranules –gelatin & acid hydrolases,
• Granules of monocytes & tissue macrophase,
a) Acid proteases,
b) Collagenase,
c) Elastase,
d) Plasminogen activator
41. Cytokines;
• Interleukins;
Active in acute inflammation – IL-1 & IL-6,
Active in chronic inflammation – IL-12 7 IL-17,
Chemokine for acute inflammation – IL-8.
• Tumor necrosis factor (TNF-α);
hepatic production of acute phase proteins,
Systemic features (fever, shock, anorexia)
• Interferons;
Activation of macrophages & NK cells
Stimulates secretion of IGs by B cell
Role in differentiation of T cells
51. GIANT CELLS;
• Giant cells are formed by fusion of variouscells.
Large in size.
Contain multiple nuclei.
phenotype depends upon the characterof cell from which
giant cell is derived.
Normally seen in
o Megakaryocytes in BM
o Syncytiotrophoblast in placenta
54. FACTOR DETERMINING VARIATION
IN RESPONSE –
Variation in response is based on host and etiologic agent.
ACUTE INFLAMMATIUON: Exception-
CHRONIC INFLAMMATION:Exception-
Typhoid
fever
acute
inflammation
Lymphocytic
infilteration
Osteomyelitis
chronic
inflammation
neutrophilic
infiltration
55. FACTOR INVOLVING THE ORGANISM;
1.Type of injury and infection
2. Virulence
3.Dose
4.Portal entry
5.Product of organism
56. FACTOR INVOLVING HOST;
1.Systemic disease
2.Immune status of host
3.Congenital neutrophil defect
4.Leukopenia
5.Site or type of tissue
6.Local host factor
57. MORPHOLOGICAL PATTERN OF ACUTE
INFLAMMATION;
1.CLASSIFICATION OF INFLAMMATORY REACTION-
A.DURATION-:
Acute –short duration ,early response
Chronic-long duration,delayed response
B.TYPE OF EXUDATE-:
1.SEROUS –when the fluid exudate resembles serum or
is watery.
2.FIBRINOUS-when the fibrin content of the fluid
exudate is high.
58. 3.PURULENT- when the formation of pus as seen in
infection withpyogenic bacteria.
4.HAEMORRHAGIC- when there is vascular damage.
5.CATARRHAL- when epithelium produces increased
secretion of mucus.
C.ANATOMICAL LOCATION OF INJURY
Eg. Solid tissue and organ(hepatitis)
Epithelium lined surface(colitis)
serous cavity (pleuritis,pericaditis)
59. 2.PSEUDOMEMBRANOUS INFLAMMATION
It is inflammatory response of mucous surface (oral,
respiratory) to toxin of diphtheria or irritant gas.
3.ULCER – it is local defect on surface of an organ produce
by inflammation .
long standing ulcer associated with fibroblastic
proliferation and scarring.
4.CELLULITIS- it is diffuse inflammation of soft tissue.
5.BACTERIAL INFECTION OF BLOOD-
Bacteraemia
Septicaemia
Pyaemia- it is a type of sepsis that leads to widespread
abscess of a metastatic nature.
62. SYSTEMIC EFFECT OF ACUTE INFLAMMATION;
1.FEVER
2.LEUCOCYTOSIS
3.ACUTE PHASE REACTANTS-
A variety of acute phase reactant protein are released in plasma in
response to tissue trauma and infection.
APRs includes the following –
a) cellular protection factor,
b) Coagulation protein,
c) Transport protein,
d) Immune agent,
e) Stress protein,
f) Antioxidant.
4.LYMPHANGITIS
5. SEPTIC SHOCK
63. OUTCOME OF ACUTE INFLAMMATION;
1.RESOLUTION- it means complete return to normal
tissue following acute inflammation.
Eg. resolution in lobar pneumonia
2.FIBROUS HEALING-
Superficial injury in More extensive tissue injury
acute inflammation causing destructive loss of tissue
Repaired by regeneration Repaired by healing with fibrosis
64. 3. SUPPURATION- when the pyogenic bacteria causing
acute inflammation result in sever necrosis,
progress to suppuration.
4.CHRONIC INFLAMMATION- recurrent acute
inflammation may progress to chronic inflammationin
which the processes of inflammation repair proceedside by
side.