This document defines inflammation and compares acute and chronic inflammation. It discusses the two types of inflammation, stimuli that cause inflammation, and the five cardinal signs of acute inflammation. The vascular events of inflammation include changes in vascular caliber and permeability that result in exudation of fluid and plasma proteins, allowing emigration of leukocytes in acute inflammation. Chronic inflammation is characterized by mononuclear cells and can lead to tissue destruction over a longer period.

1. Dr SHARIFF M H
PROFESSOR
DEPT OF PATHOLOGY

2.  Definition of Inflammation
 Two Types of Inflammation
 Cause / stimuli of Inflammation
 Five Cardinal Features of Acute Inflammation
 Comparision of Acute Vs Chronic Inflammation
 Vascular events of Inflammation
1. Change in Vascular Caliber
2. Change in Vascular Permeability
 Difference between Transudate & Exudate

3.  Inflammation:
Protective response intended to eliminate the initial
cause of cell injury, the necrotic cells and tissues
(result arising from) the injury
 Inflammation is also intimately associated with
the repair process which includes parenchymal
cell regeneration and scarring

4.  Acute
 Chronic

5. Comparision
ACUTE CHRONIC
Duration Early (Short term)
Min to days
Reaction that lasts
for months or years
Specificity Not specific Specific : Acquired
immunity
Type of Cells PMN’S Lymphocytes &
macrophages
(Mononuclear)
Response Triple Response Fibrosis &
Angiogenesis
Signs Cardinal Signs No Cardinal signs
Characterised by Fluid & Protein
(Exudate)

6.  Acute - minutes to days
◦ Characterized by fluid and protein
◦ PMN’s
◦ Exudate SG > 1.020
 Chronic - weeks to years
◦ Lymphocytes and macrophages
 ACUTE Inf - PMN’s (Polymorphonuclear cells)
 CHRONIC Inf - Mononuclear Cells
EXUDATE

7. 1. INFECTIONS – Bacterial,
viral,
fungal,
parasitic &
Microbial Toxins
2. TISSUE NECROSIS –
ischemia (MI),
trauma,
physical
chemical injury,
Thermal (burns, Frost bites, irradiation) injury,
3. FOREIGN BODIES – splinters, dirt, sutures
4. IMMUNE REACTIONS – autoimmune diseases.
Immune mediated inflammatory disease.

8. ◦ Heat
◦ Redness
◦ Swelling
◦ Pain
◦ Loss of function
◦ Calor – vasodilatation
◦ Rubor – vasodilatation
◦ Tumor – vascular permeability
◦ Dolor – mediator release/PMNs
◦ Functio laesa – loss of function

9.  Rubor = redness
 Tumor = swelling
 Calor = heat
 Dolor = pain ( Celsus 1st. Century AD)
 Functio laesa = loss of function
( R. Virchow)
Cellulits = acute skin infection commonly
caused by Streptococcus pyogenes or
Staphylococcus aureus

11.  Rapid host response that serves to deliver
leukocytes and plasma proteins at site of
infection/injury
 2 Events
 Vascular Events
 Cellular Events

12. Vascular Events

13.  CHANGES IN VASCULAR CALIBER
 INCREASED VASCULAR PERMEABILITY
 RESPONSES OF LYMPHATIC VESSELS

14. CALIBER
 Vasoconstriction (Initial & Transient)
 Vasodilation : Prolonged
PERMEABILITY
 Exudation of protein rich fluid
 Blood stasis
 Margination
 Emigration/Transmigration

15. Vascular changes
Protein exits vessels :
 intravascular hydrostatic pressure
 intravascular osmotic pressure
Endothelial gaps at intercellular junctions:
release of histamine, bradykinin,
leukotrienes, substance P

18.  Vasodilation – increased blood flow
↑ intravascular hydrostatic pressure
 Transudate - ultrafiltrate blood plasma
( ↓ protein)
◦ Again, this is very transient and just gets the
process started. Think acute inflammation, think
EXUDATE
 Exudate - (↑ protein with PMNs)
 Intravascular osmotic pressure
 ↑Osmotic pressure of interstitial fluid
 Outflow of water and ions - edema

19. EXUDATE TRANSUDATE
 Grossly : Turbid / Cloudy Clear / Watery
 Specific
Gravity
>1.015 <1.015
 PROTEIN > 3mg/dL <3mg/dL
 Cholesterol >1.2mmol/L <1.2mmol/L
 Cellularity Hypercellular Hypocellular
 IMPLIES Increased Permeability &
Lymphatic Obstruction
IMBALANCE BET.OSMOTIC &
 HYDROSTIC PRESSURE

20.  Endothelial cell contraction—histamine binds to endothelial cell
receptors causing the endothelial cells separate
 Direct endothelial injury (immediate sustained response)--
Endothelial cell necrosis and detachment. Result of severe injury or burn.
Occurs immediately and lasts until vessel repaired
 Leukocyte-dependent endothelial injury—Leukocytes adhere to
endothelium, and release toxic oxygen species which cause
endothelial injury.
 ↑Transcytosis of fluid—VEGF increases the size/number of
endothelial channels. The channels consist of vesicles and vacuoles.
 Leakage from new blood vessels– During repair, there is
angiogenesis. New vessels remain leaky.

21. © 2005 Elsevier

22.  LYMPH FLOW IS INCREASED AND HELPS DRAIN
EDEMA FLUID
 PROLIFERATION OF LYMPHATIC VESSELS
 LYMPHANGITIS
 LYMPHADENITIS
 REACTIVE /INFLAMMATORY LYMPHADENITIS:
constellation of pathologic changes.

23.  ESSENTIAL FOR SURVIVAL
 FUNDAMENTALLY PROTECTIVE RESPONSE
 COMPLEX REACTION OF VASULARISED TISSUE
TO INJURY
 CONSISTS OF RESPONSES OF BLOOD VESSELS
AND LEUKOCYTES

24.  EVENTS ARE TRIGGERED BY SOLUBLE
FACTORS DERIVED FROM VARIOUS CELLS /
PLASMA PROTEINS
 2 TYPES: ACUTE AND CHRONIC
 ACUTE : RAPID ONSET, SHORT DURATION,
EXUDATION OF FLUID AND PLASMA PROTEINS
AND EMIGRATION OF LEUKOCYTES
 CHRONIC: INSIDUOUS ONSET, LONGER
DURATION WITH TISSUE DESTRUCTION

25.  INFLAMMATION IS TERMINATED WHEN THE
OFFENDING AGENT IS ELIMINATED
 INFLAMMATORY PROCESS IS INTERTWINED
WITH THE PROCESS OF REPAIR
 INFLAMMATION MAY BE HARMFUL IN SOME
SITUATIONS
 IT MAY CONTRIBUTE TO A VARIETY OF
DISEASES LIKE DIABETES, ALZHEIMER DISEASE
– “SILENT KILLER”

27. I. Vasodialation – histamine and NO
II. Increased microvasculature permeability
III. Stasis and congestion
IV. Accumulation of neutrophils along
endothelium

28.  3 major components
1. Alteration in vascular caliber
2. Structural changes in the microvasculature
3. Emigration of leukocytes