2ND BAMS

1. LECTURE ON
:INFLAMMATION
BY
Dr . Prashanth Jain
M.D(Ayu)

2. DEFINE INFLAMMATION

3. INFLAMMATION
 Inflammation is a body defence reaction in order to
eliminate or limit the spread of injurious agent as well as
to remove the necrosed cells .
 It is local response of living mammalian tissues to
injury due to any agent.

4. Inflammation serves to destroy, dilute or isolate
the injurious agent (microbes, toxins) and
eliminate the necrotic cells and tissues.
Inflammation is part of a broader protective
response (innate immunity )
It starts a series of events which leads as far as
possible to the healing and reconstitution of the
damaged tissue.

5. CAN INFLAMMATION CAUSE
CONSIDERABLE HARM TO THE BODY?
They may induce harm
e.g. anaphylactic reaction
rheumatoid arthritis
atherosclerosis
pericarditis

6. CAUSES OF ACUTE INFLAMMATION
 Triggered by a variety of stimuli:
Infections (bacterial, viral, parasitic) and microbial
toxins
 Trauma (blunt and penetrating)
 Physical and chemical agents (thermal injury,
e.g., burns or frostbite; irradiation; some
environmental chemicals)
 Tissue necrosis (from any cause)
 Immune reactions (also called hypersensitivity
reactions)

7. IMPORTANT ROLES IN
INFLAMMATION
blood leukocytes
plasma proteins
cells of vascular walls
cells of the surrounding connective tissue
extracellular matrix (ECM) of the surrounding
connective tissue

8. The
connective
tissue cells
The circulating cells:
The
extracellular
matrix

9. Cells and molecules that play important roles in inflammatCells and molecules that play important roles in inflammat

10. Tissues and cells involved in inflammatory response :
The fluid and proteins of plasma, circulating cells, blood vessels
and connective tissue
•The circulating cells: neutrophils, monocytes, eosinophils,
lymphocytes, basophils, and platelets.
• The connective tissue cells are the mast cells, the connective
tissue fibroblasts, resident macrophages and lymphocytes.
•The extracellular matrix, consists of the structural fibrous
proteins (collagen, elastin), adhesive glycoproteins
(fibronectin, laminin,), and proteoglycans

11. CARDINAL SIGNS OF INFLAMMATION?

12. CARDINAL SIGNS
Celsus described the local reaction of injury in
terms that have come to be known as the
cardinal signs of inflammation.
These signs are:
 rubor (redness)
 tumor (swelling)
 calor (heat)
 dolor (pain)
 functio laesa, or loss of function (In the second century
AD, the Greek physician virchow added this fifth cardinal
sign)

14. WHAT ARE TYPES OF INFLAMMATION?

15. Acuteinflammation.
Chronic inflammation.

16. SYSTEMIC EFFECTS OF ACUTE
INFLAMMATION
 Fever
 Leucocytosis
 Lymphadenitis
 shock

17. SYSTEMIC EFFECTS OF CHRONIC
INFLAMMATION
 Fever
 Anaemia
 Leucocytosis
 Elevated ESR

18. CHRONIC INFLAMMATION:TYPES
 NON SPECIFIC: chronic osteomyelitis ,chronic
ulcer
 SPECIFIC: tuberculosis,leprosy , syphilis

19. WHAT IS THE DIFFERENCE BETWEEN
THESE TYPES OF INFLAMMATION?

20. ACUTE
INFLAMMATION
 rapid in onset (seconds or
minutes)
 relatively short duration,
lasting for minutes, several
hours, or a few days
 its main characteristics:
 the exudation of fluid and
plasma proteins (edema)
 the emigration of
leukocytes, predominantly
neutrophils.
 is of longer duration
 associated histologically with
the presence of lymphocytes
and macrophages, the
proliferation of blood vessels,
fibrosis, and tissue necrosis.
Chronic inflammation

21. WHAT IS THE SOURCE OF CHEMICAL
MEDIATORS IN INFLAMMATION?

22. SOURCE OF CHEMICAL MEDIATORS
IN INFLAMMATION
 Phagocytes and other host cells
 Leukocyte
 Endothelium
 Mast cell
 Plasma proteins

23. WHAT IS THE ACTION OF CHEMICAL
MEDIATORS IN INFLAMMATION?
Some of mediators act on small blood
vessels
Recruitment of circulating leukocytes to
the site where the offending agent is
located

24. THE STEPS OF THE INFLAMMATORY
RESPONSE WHICH CAN BE
REMEMBERED AS THE FIVE R:

25. STEPS OF THE INFLAMMATORY
RESPONSE
(1) Recognition of the injurious agent
(2) Recruitment of leukocytes
(3) Removal of the agent
(4) Regulation (control) of the response
(5) Resolution

26. WHAT ARE THE TWO MAJOR COMPONENTS
OF ACUTE INFLAMMATION?

27. COMPONENTS OF ACUTE
INFLAMMATION
 Vasodilation:
alterations in vessel
caliber resulting in
increased blood flow
 Increased vascular
permeability: permit
plasma proteins to
leave the circulation
 Emigration of the
leukocytes from the
microcirculation and
accumulation in the focus
of injury
 Principal leukocytes in
acute inflammation are
neutrophils
(polymorphonuclear
leukocytes).
Vascular changes Cellular events

29.  Acute inflammation is a rapid response to an injurious
agent that serves to deliver mediators of host defense-
leukocytes and plasma proteins-to the site of injury.

30. VASCULAR CHANGES
(1) Hemodynamic changes
(alterations in vascular caliber that lead to an
increase in blood flow)
(2) Increased vascular permeability

31. VASCULAR CHANGES
1. Transient vasoconstriction of arterioles
- It disappears within 3-5 seconds in mild injuries
- It may last several minutes in more severe injury (burn)

32. 2.Persistant progressive Vasodilatation:
Leads to increased blood flow (reason for redness
and warmth)
.
Increased blood volume lead to increased local
hydrostatic pressure leading to transudation of
protein - fluid into the extravascular space.(reason
for swelling)

33. 3. Slowing and stasis of the
microcirculation: due to increased permeability
of the microvasculature, this leads to outpouring of
protein-rich fluid in the extravascular tissues.
This results in concentration of the red cells in small
vessels and increased viscosity of the blood leading
to stasis
(stasis: slow circulation due to dilated small vessels
packed with red cells).

34. 4. leukocyte margination
persistant stasis leads to peripheral orientation of
leukocytes (mainly neutrophils) along the vascular
endothelium [leukocytic margination], then they
migrate through the vascular wall into the interstitial
tissue [emigration].

35. CELLULAR RESPONSE
 The cellular response of acute inflammation is marked by
movement of phagocytic white blood cells (leukocytes) into
the area of injury.
 Two types of leukocytes participate in the acute
inflammatory response - the granulocytes and monocytes.
 The sequence of events in the cellular response to
inflammation includes:
 pavementing
 emigration
 chemotaxis
 phagocytosis

36. MARGINATION AND
PAVEMENTING
 Normally RBC are central and leucocytes reside near to
vessels.
 Due to slowing down of blood ,RBC get grouped up pushing
leucocytess even closure to periphery around endothelial
surface .
 This process of leucocyte accumulation is called
margination.
 Rows of leucocytes along the endothelium finally coming to
rest at some point where they adhere firmly called as
pavementing

37. EMIGRATION AND CHEMOTAXIS
 Emigration is a mechanism by which the leukocytes
extend pseudopodia, pass through the capillary walls by
ameboid movement, and migrate into the tissue spaces.
 The emigration of leukocytes also may be accompanied by
an escape of red blood cells.
 The process by which leukocytes migrate in response to a
chemical signal is called chemotaxis.

38. PHAGOCYTOSIS
 Phagocytosis: is defined as process of engulfment of solid
particulate material by cells. cells performing this function are
called phagocytes
 1)polymorphonuclear neutrophils (microphages)
 2)circulating monocytes called as macrophages
Phagocytosis involves distinct steps:
 Recognisation and attachment stage(opsonisation)
 Engulfment stage
 Digestion and degradation stage/killing stage

39. RECOGNITION AND ATTACHMENT
STAGE:
 In order to establish a bond between
bacteria and cell membrane of phagocytic
cells ,the micro oragnisms get coated with
opsonins which are naturally occuring
factors in serum.

40. PHAGOCYTOSIS