Inflammation Presentation ...

1. “INFLAMMATION”
Dr.Zulcaif Ahmad
+92 03204998472

2. INTRODUCTION
• It is derived from LATIN word
meaning ignite.
• It literally means flaming, burning
Defination:
“It refers to reaction of living
tissue to all forms of injury, and
involves vascular, neuralgic,
humoral & cellular response at
the site of injury.”

3. “NOMENCLATURE OF
INFLAMMATION”
• The nomenclature used to
describe inflammation in
different tissues employs the
tissue name & suffix “itis”.
• Example:
pancreatitis
nephritis
appendicitis & etc.

4. Clinical Significance
“It is a protective or defensive
process why?”
• it removes or destroys causative agents
• Repairs tissue damage
• Inactivate toxins
• Prepare tissue or organ for healing & repair

5. WITHOUT INFLAMMATION??
• Infections would go unchecked.
• Wounds would never heal.
• Injured organs may remain permanently
damaged.

6. “TYPES OF INFLAMMATION”
• On the basis of severity, duration,
onset &other factors it can be
categorized as,
1) Acute inflammation
2) Chronic inflammation

7. Acute Inflammation
• “The acute inflammatory response rapidly
delivers leukocytes and plasma proteins to
site of injury. once there leukocytes clear
the invaders and begins the process of
digesting and getting rid of necrotic
tissue.”
• Cells of Acute Inflammation:
• Neutrophils (for first 24-48 hours)
• Macrophages (after 48 hours)

8. ETIOLOGY OF ACUTE
INFLAMMATION
• MECHANICAL TRAUMA: cutting or crushing
• CHEMICAL INJURY: corrosive acids, alkalis,
phenol, general poisons.
• RADIATION INJURY: heat, UV light, all forms of
ionizing radiations.
• INJURY DUE TO COLD AND HEAT
• INJURY BY LIVING ORGANISM: infection by
viruses, bacteria & larger parasites.

9. • INJURY DUE TO IMMUNOLOGICAL
MECHANISM: diseases mediated by Ag-
AB interactions
• Hypoxia
• BURNS
• TOXINS
• STRESS
• CHEMICAL IRRITANTS etc.

10. Internal View & External View
Of Rubor.

11. DOLOR Tumor

12. FUNCTIO LAESA

13. .

15. CELLULAR EVENTS OF
ACUTE INFLAMMATION
• Vascular changes (Vasodilation, inc.
vascular permeability)
• Cellular events takes place such as;
 MARGINATION
ADHESION
EMIGRATION
CHEMOTAXIS
PHAGOCYTOSIS

16. Process of acute inflammation
Initiated by cells
already present
Cells present on
surface receptor
(PRRs)Pattern
recognition
receptor
Distinguish from
host cell
(PAMP) Pathogen
assosiated
molecular
patterns
Onset of
infection burn or
injury
Cell undergo
activation and
release mediator
Vasodilation
Increased blood
flow

17. Causes redness
& heat
Inc.permeability
of blood vessels
result
Exudation
(leakage) of
plasma protein
And fluid into
tissue
Manifests itself
as swelling
Some mediator
such as
bradykinin
Mediator alter the
migration of
leukocytes
Mainly neutrophil
& macrophages
out side he
b.vessels
Neutrophils
migrate along
chemotactic
gradient

18. Reach the site
of injury
Loss of
function result
of neurological
reflex
Inflammation
ceased once
the stimuli has
been removed

20. Triple response
• LEWIS in 1942 noted that firm stroking of a
human skin results in a triple response.
The features of this response are
RED LINE: it is sharply demarcated red
line at the site of stroking due to capillary
dilation.
THE FLARE: after 15-30sec flare appears
surrounding a line due to arteriolar dilatation.
THE WEAL: on the site of red line a wheel
subsequently appears due to exudation of
fluid through vessel wall.

21. “EXUDATION”
• EXUDATION:
“The escape of fluid, cells, and cellular debris
from blood vessels and their deposition in or
on to the tissues as result of inflammation is
known as exudation.”
• Exudate:
“It is an inflammatory extravascular fluid that
has high protein conc., much cellular debris
which leaks from vessels into the interstitial
space due to increased vascular
permeability.”

22. MEDIATORS OF ACUTE
INFLAMMATION
• MEDIATORS:-
These are the chemical substances that
trigger certain process in an inflammation.
TYPES OF MEDIATORS:
1. Histamine
2. Serotonin
3. NEUTROPHILIC PROTEASES
4. ADRENALINE AND NOR ADRENALINE
5. The kinins
6. Plasmin

23. 7)DERRIVATIVES OF ARACHIDONIC ACID(AA)
– THE PROSTAGLANDINS
– LEUKOTRIENES
8) PLATELET ACTIVATING FACTOR (PAF)
9) CYTOKINES
10) LYSOSOMAL CONTENTS OF
NEUTROPHILS
11) COMPLEMENT SYSTEM
12) OTHER MEDIATORS:
NEUROPEPTIDES
NITRIC OXIDE:

24. OUTCOMES OF ACUTE
INFLAMMATION
• COMPLETE RESOLUTION
• SCARRING OR FIBROSIS
• ABCESS FORMATION
• PROGRESSION TO CHRONIC
INFLAMMATION

25. • SCARRING
*ABCESS
CHRONIC INFLAMMATION

26. SPECIAL TYPES OF ACUTE
INFLAMMATION
On principle components of exudates, acute
inflammation has followimg types:
1. Serous Inflammation
2. Fibrinous Inflammation
3. Suppurative Inflammation
4. Abcess Forming Inflammation
5. HEMORRHAGIC INFLAMMATION

27. CHRONIC INFLAMMATION
• It is the prolong response of the body to the
persistent injurious stimulus and is characterized
by:
• Infiltration with mononuclear cells.
• Tissue destruction.
• Repair.
• CHRONIC INFLAMMATORY CELLS
• Lymphocytes
• Macrophages
• Plasma cells

28. ETIOLOGY
• Unresolved acute inflammation:
Due to persistence of injurious agent
interference of normal process of healing
• Chronic inflammation without acute
phase:
It may start from the very beginning
Such type of injurious agents are of low
toxicity in comparison of those that lead to
acute inflammation.

29. CAUSES
1. CHRONIC VIRAL INFECTIONS:
chronic viral hepatitis
2. CHRONIC AUTOIMMUNE DISEASES:
rheumatoid arthritis
3.CHRONIC CHEMICAL INTOXICATION:
chronic alcoholic liver disease
4.ALLERGIC INFLAMMATION:
bronchial asthma

30. TYPES
1) GRANULOMATOUS CHRONIC
INFLAMMATION
2) NON GRANULOMATOUS CHRONIC
INFLAMMATION

31. GRANULOMATOUS
• This type of chronic inflammation is
characterized by formation of epithelioid
cells & granuloma
• GRANULOMA:
A collection of modified macrophages
resembling epithelial cells, usually
surrounded by a rim of lymphocytes.

32. NON GRANULOMATOUS
It is characterised by accumulation of:
• Sensitized lymphocytes
• Plasma cells
• Macrophages in the injured area.
• Cells are scaterred throughtout the tissues
• Do not form granulomas
• Scaterred tissue necrosis and fibrosis are
common.

33. FEATURES ACUTE CHRONIC
• DURATION Short (days) Long (weeks-
months)
• ONSET Acute Insidious
• INFLAMMATORY
CELLS
Neutrophils,
macrophages
Lymphocytes,plasma
cells,macrophages &
fibroblasts
•VASCULAR
CHANGES
Active vasodilation,
increased
permeability
New vessel formation
“granulation tissue”
•FLUID
EXUDATION
Present Absent
•CARDINAL Present Absent

34. REFERENCES
• COLOR ATLAS OF PATHOLOGY BY
URUS.
• GROSS PATHOLOGY BY JAWAD
AHMED.
• GENERAL PATHOLOGY BY ROBIN’S
AND CARTON’S.
• GENERAL PATHOLOGY BY WALTER
AND ISRAEL.
• SHORT TEXTBOOK OF PATHOLOGY
BY INAM DANISH.