https://userupload.net/sjs4xysersdu Acute inflammation is a short-term process occurring in response to tissue injury, usually appearing within minutes or hours. It is characterized by five cardinal signs: pain, redness, immobility (loss of function), swelling and heat. Acute inflammation is a short-term process occurring in response to tissue injury, usually appearing within minutes or hours. It is characterized by five cardinal signs: pain, redness, immobility (loss of function), swelling and heat. The acute inflammatory response is composed of an elaborate cascade of both proinflammatory and anti-inflammatory mediators.

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2. References :
1)KUMAR,COTRAN,ROBBINS-BASIC
PATHOLOGY (7th
edition)
2)ESSENTIAL PATHOLOGY-
HARSHMOHAN (4th
edition)
3)INFLAMMATION-a review of the
process.Henry O. Trowbridge,Robert
C.Emling(5th
edition)

3. Contents
 Introduction
 Definition and causes
 Acute inflammation
 Vascular changes
 Leukocyte cellular events
 Chemical mediators of inflammation
 Systemic effects of inflammation
 Outcome of Acute inflammation

4. INTRODUCTION
The word inflammation is derived from the state of
being inflammed
To inflamme to set a fire
French - enflamme
Latin - inflammare
Inflammation and reparative responses are fundamental
to survival of the organism.

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6. Inflammation is defined as the local response of vascularized living
tissues to local injury due to any agent (ROBBINS)
Inflammation is a protective response intended to
eliminate the initial cause of injury as well as necrotic
cells and tissues resulting from original insult.
Agents causing inflammation :
Physical agents
Chemical agents
Infective agents
Immunological agents
Definition and causes

7. Thomas Lewis demonstrated that inflammation is
brought about by chemical mediators, most of which act
locally. Lewis induced changes in the skin of inner
aspect of forearm by firm stroking with a blunt point
(1) an immediate red scratch mark;
(2) a red flare around the scratch mark;
(3) a red swollen area ("wheal") around the
flare.

8. Lewis Triple
Response
•FlushFlush:: capillary
dilatation.
•FlareFlare:: arteriolar
dilatation.
•WhealWheal:: exudation,
edema.

9. SIGNS OF INFLAMMATION
The cardinal signs of inflammation
a. Rubor {redness}
b. Calor {heat}
c. Tumor {swelling}
d. Dolor {pain}
e. Functio laesa {loss of function}

11. Divided into 2 basic patterns :
Acute inflammation
Chronic inflammation

12. Acute inflammation v/s chronic inflammation
Distinguished not only by the time course
of inflammatory response but also but H/P
Acute inflammation- which is typical of early phases of
the inflammatory response involves
polymorphonuclear neutrophil leukocytes as the
principal cells and cellular effectors.
Chronic inflammation -which tends to occur over a
longer duration involves monocytes, lymphocytes ,
macrophages, and plasma cells (collectively
mononuclear leukocytes).

13. Acute inflammation
Immediate and early response designed to deliver leukocytes to
the site of injury
Two major components-
Vascular changes:
Changes in the vascular caliber and flow
Increased vascular permeability
Cellular events:
Margination and Rolling
Adhesion and Transmigration
Chemotaxis and Activation
Phagocytosis and Degranulation

14. Changes in the vascular caliber and
flow

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16. Starling’s law
The movement of fluid in and out of
arterioles, capillaries and venules is
regulated by the balance between
intravascular hydrostatic pressure ,which
tends to force fluid out of the vessels,and
the opposing effects of osmotic pressure
exerted by the plasma proteins, which tends
to retain fluid within the vessels.

17. Blood pressure and plasma colloidal
osmotic forces in normal and inflammed
microcirculation

18. • Most common
• Post-capillary venules
• Reversible process elicited
by histamine, bradykinin,
leukotrienes, and many other
chemical mediators
• Rapid and short-lived
reaction (minutes)
• Immediate transient
response
Increased vascular permeability
Endothelial cell contraction
Endothelial cell retraction: TNF
IL-1

19. Direct endothelial injury
• Arterioles, capillaries
and venules
•Toxins,burns,chemicals
• Fast and may be long
lived (hours to days)
• Immediate, sustained
response

20. Leukocyte mediated endothelial injury
•Venules
•Pulmonary capillaries
•Late response
•Long lived (hours)

21. Increased transcytosis and angiogenesis

22. Cellular events
 Margination and rolling
 Adhesion and transmigration
 Chemotaxis and activation
 Phagocytosis And Degranulation

24. Margination and Rolling

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26. Adhesion and Transmigration
Leukocytes firmly adhere to endothelial cells before diapedesis
Adhesion is mediated by members of Ig superfamily on endothelial
cells (ICAM-1, VCAM-1) that interact with leukocyte integrins
(VLA-4, LFA-1). Diapedesis typically occurs in venules and is
mediated by PECAM-1 (CD31), also of Ig superfamily

27. Transmigration
Summary : endothelial activation
leukocyte rolling
firm adhesion
transmigration

29. Chemotaxis and activation
Transmigrated leukocytes move to the site of
injury
along chemical gradients of chemotactic agents
Chemotactic agent can be:
-Soluble bacterial products (N-
formylmethionine termini)
-Components of the complement system (C5a)
- Products of lipoxygenase pathway of
arachidonic acid metabolism (leukotriene B4)
- Cytokines (chemokines such as IL-8)

30. Biochemical events in leukocyte activation

31. Phagocytosis and degranulation
-Phagocytosis consists of three distinct but
interrelated steps :
1. Recognition and attachment of the particle to the
ingesting leukocyte.
2. Engulfment with subsequent formation of a
phagocytic vacuole
3. Killing and degradation of the ingested material

33. Phagocytosis,degranulation and
oxygen dependent antimicrobial
activity
The dead microorganisms are then degraded by action of lysosomal
acid hydrolases

35. Chemical mediators of inflammation
Mediators may be circulating in the plasma or they may
be produced locally by cells at the site of inflammation
Most mediators induce their effects by binding to
specific receptors on target cells.
Mediators may stimulate target cells to release
secondary effector molecules.
Mediators may act only 1 or a very few targets,or they
may have widespread activity
Mediator function is tightly regulated

37. Interrelationships between the four plasma
mediator systems triggered by activation of
Hageman factor

38. Arachidonic acid formation and its
role in inflammation

39. Vasoactive amines
Histamine…released in response to
1. Trauma or heat
2. Immune reactions involving IgE antibodies binding..
3. Anaphylatoxins
4. Leukocyte derived histamine releasing protein
5. Neuropeptides
6. Cytokines(IL-1,IL-8)
Serotonin…
Neuropeptides: substance P
Plasma proteases

40. Complement system
Cascade Of Plasma Proteins….
Function By Generating MAC
Complement Components(C1 To C9)..In Plasma
Biologic Function is activation Of C3
Complement Derived Factors In Inflammation :
Vascular Effects : C3a And C5a- Increased Vascular
Permeability
Vasodilation
Leukocyte activation,adhesion And Chemotaxis-C5a
Phagocytosis: C3b as opsonin

41. CYTOKINES
Polypeptide products of many cell types that modulate the
function of other cell types
-Colony stimulating factor
-Classic growth factors
-Interleukins
-Chemokines
-produced during immune and inflammatory responses.
-secretion is typically transient and tightly regulated
-effects tend to be pleiotrophic

42. CYTOKINES EXHIBIT
-Autocrine effect
-Paracrine effect
-Endocrine effect
Based on their action on target cells –
Cytokines that regulate lymphocyte function-IL-2, TNF-BETA
Cytokines involved in innate immunity :TNF,IL-1
Cytokines that activate inflammatory cells during cell mediated immune
responses::
IFN-alpha,IL-12
Cytokines that have chemotactic activity for various leukocytes
Cytokines that stimulate hematopoiesis-GM-CSF
IL-3

43. CHEMOKINES
-small proteins that act as activators and
chemoattractants for subsets of leukocytes
-maintain the chemoattractant gradient necessary
for the directed migration of recruited cells.
-mediate their activities by binding to specific G
protein-coupled receptors on target cells
There are 4 general types of chemokines with
distinct biological activities.

44. SOURCES AND EFFECTS OF NITRIC
OXIDE IN INFLAMMATION

45. Platelet activating factor : potent vasodilator also increases
vascular permeability
Induction of platelet aggregation at the site of tissue injury
Release of serotonin by platelets
Lysosomal constituents :
• -contain multiple molecules that can mediate acute
inflammation.
Released after cell death
leakage during phagocytic
vacuole
• Include: acid proteases
neutral proteases(elastase,collagenase,cathepsin)
antiproteases: alpha2- macrogobulin, alpha1-
antitrypsin

46. Effects of inflammation and their major mediators
Vasodilation –PG’s, NO
Increased vascular permeability- Vasoactive amines ,C3a and C5a
Bradykinin , Leukotrienes,
PAF
Chemotaxis,leukocyte activation- C5a, leukotriene B4
bacterial products
Chemokines
Fever - IL-1,IL-6,TNF
Pain - PG,bradykinin
Tissue damage – Neutrophil and macrophage lysosomal enzymes
Oxygen metabolites
NO

47. Systemic effects of acute inflammation
Pyrexia : Polymorphs and macrophages produce
compounds known as endogenous pyrogens
Release of endogenous pyrogens is stimulated by
phagocytosis, endotoxins and immune complexes.
Constitutional symptoms: malaise,anorexia,nausea
Reactive hyperplasia of the reticulo-endothelial system
Local or systemic Iymph node enlargement
commonly accompanies inflammation, while
splenomegaly is found in certain specific infections
(e.g. malaria, infectious mononucleosis).
Haematological changes
Increased erythrocyte sedimentation rate.
Leukocytosis.

48. Outcomes of acute
inflammation
Resolution
Scarring & fibrosis
Progression to chronic inflammation

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