Acute inflammation is the body's initial response to harmful stimuli and involves both vascular and cellular events. The vascular events include increased blood flow, vascular permeability and blood vessel dilation. The cellular events include the recruitment of leukocytes from the bloodstream to the site of injury and their migration into tissues. This is followed by phagocytosis of pathogens and damaged cells by macrophages and neutrophils. Mediators of acute inflammation such as histamine, cytokines and complement proteins are released from cells to promote the inflammatory response. The response and its outcomes can vary depending on factors related to the host and the causative agent.

1. ACUTE INFLAMMATION

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

4. SIGNS OF INFLAMMATION

5. TYPES OF INFLAMMATION

6. ACUTE
INFLAMMATORY
RESPONSE
• Vascular events
• Cellular events

7. VASCULAR EVENTS;
HAEMODYNAMIC
CHANGES
ALTERED VASCULAR
PERMEABILITY

8. HAEMODYNAMIC CHANGES;
Transient
vasoconstriction
of arterioles
Persistent
progressive
vasodilation
Increased
hydrostatic
pressure
Stasis of
microcirculation
Leucocytic
margination

9. TRIPLE RESPONSE

10. ALTEREDVASCULAR
PERMEABILITY

11. StarliNg hypothesis;
FORCES CAUSING
OUTWARD
MOVEMENT
• Intravascular
hydrostatic pressure
• Colloid osmotic
pressure of interstitial
fluid
FORCES CAUSING
INWARD
MOVEMENT
• Intravascular colloid
osmotic pressure
• Hydrostatic pressure
of interstitial fluid

12. Fluid exchange between blood &
extracellular fluid;

13. Mechanism of
vascular leakage;

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

17. ROLLING AND ADHESION;
MEDIATORS:
SELECTINS
 P-SELECTIN
 E-SELECTIN
 L-SELECTIN
INTEGRINS

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

23. Engulfment;
Cytoplasmic
pseudopods
formation
Phagosome is
internalise

24. KILLING & DEGRADATION;
Mechanisms involved
A. Intracellular mechanisms
B. Extracellular mechanisms

25. Intracellular
mechanism;
Reactive oxygen species

26. Nitric oxide
Lysosomal granules

27. Extracellular mechanisms;
Activated leucocytes
Neutrophill extracellular traps
Immune mechanisms

28. Mediators Of Acute
Inflammation

29. These are endogenous,
Chemical substances
which mediate the
process of acute
inflammation.

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

35. Mediators of inflammation;

36. CELL DERIVED MEDIATORES;
Vasoactive
amines
Lysosomal
components
Arachidonic acid
metabolites
Cytokines
Free radicals& NO
Platelet
activating
factors
Preformed/stored Freshly formed

37. Vasoactive amines;
• Histamine;
Source- mastcell, bronchus, platelets.
Functions,
Degranulations.
• Serotonine (5-HT);
Source-
enterochromaffin cell, platelets
Functions.
• Neuropeptides;
SubstanceP,
Neurokinins A,
Vasoactiveintestinal peptide(VIP),
Somatostatin.

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

39. Arachidonic acid metabolites
via cyclooxygenase pathway

40. Arachidonic acid metabolites
via lipooxygenase pathway

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

42. Nitric oxide [NO];
L- arginine NO
Guanylate cyclase Inhibits Calcium channel
cGMP
Smooth muscle relaxation
vasodilation
NOS
eNOS iNOS nNOS

43. PLASMA PROTEIN DERIVED;
The kinin system
The clotting
system
The fibrinolytic system
The
complement
system

44. PATHWAY OF KININ SYSTEM;
Factor XII
Factor XIIa
Prekallikrein activator
Plasma Prekallikrein kallikrein
kininogen BRADYKININ
Endothelium damage& exposure
of collagen fibres
Smooth muscle
contraction
Vasodilation
Increased vascular
permeability
pain

45. PATHWAY OF THE CLOTTING SYSTEM;
FDPs
fibrinopeptides
Increased vascular
permeability
Chemotaxis for
leukocytes
Anticoagulant
activity

46. THE FIBRINOLYTIC SYSTEM;
Plasminogen activator
(kallilrein, XIIa, leucocytes, endothelium)
Plasminogen Plasmin
Activation ofXII C3 fibrin
bradykinin C3a
Fibrin degradation
products

47. Complement system;
• Responsiblefor immunity,
• 10-20 % of plasma proteins,
• C1 to C9 complementprotein with multiplesubunits,
C3
C3a
C3b
C5
C5a
C5b
Anaphylatoxins
Opsonisation
Anaphylatoxins,
chemotaxis
MAC formation
• Classical pathway
• Lectin pathway
• Alternatepathway

48. Complement pathway;
Classical pathway;
Associated with IgG & IgM antibodies
Alternate pathway;
Associated with IgA, endotoxinsand venoms
C1 Activated C1
C4 / C2 C4b2a
C3 break down
C3a C3b
C4b2a3b C5 breakdown
C5a C5b
C3 + factor B
C3bBb
C6/7/8/9
C5b-9 complex
Membrane attacking complex

49. INTERRELATIONSHIP AMONG
DIFFERENT SYSTEM;

50. INFLAMMATORY 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

52. Types of giant cells;
1. Macrophagederived giant cells
Langhan’s GC
Foreign body GC
Touton GC
Aschoff GC
2. Epidermal cell derived giant cells
Tzanck GC
Multinucleated epidermal GC

53. ACUTE INFLAMMATION -FACTORS
DETERMINING VARIATION IN
RESPONSE, MORPHOLOGIC
PATTERN, SYSTEMIC EFFECTS
AND OUTCOMES

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.

60. 6.SUPPURATION(ABSCESS FORMATION)
Acute bacterial infection
Neutrophillic infiltration in inflammed tissue
Tissue necrosis
Cavity is formed
Abscess formation
(SUPPURATION)

61. Abscess
Formation

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.