1. INFLAMMATION
DEFINITION
INFLAMMATION IS A HOST RESPONSE TO LOCAL
INJURY IN VASCULARISED TISSUES.

2. CARDINAL SIGNS OF INFLAMMATION
•

3. INFLAMMATION- CARDINAL SIGNS: CELSUS
 RUBOR-REDNESS
 CALOR-HEAT
 TUMOR-SWELLING
 DOLOR- PAIN
 5TH SIGN DESCRIBED BY VIRCHOW-LOSS OF FUNCTION
(FUNCTIO LAESA)

4. INFLAMMATION-TYPES
ACUTE CHRONIC
Onset Rapid Slow
Duration Short Longer
Predominant Neutrophil Lymphocytes and
cells macrophages
Chief Exudation of fluid Proliferation of
pathological and plasma blood vessels and
event proteins fibrosis

5. INFLAMMATION-STIMULI
 Infection- bacterial, viral , parasitic
 Trauma
 Physical/chemical injury- burns, irradiation
 Tissue necrosis
 Foreign body
 Immune reaction

6. ACUTE INFLAMMATION
 VASCULAR CHANGES:
 Vascular caliber alteration.
 Change in vascular structure.
 CELLULAR EVENTS:
 leucocyte emigration

8. ACUTE INFLAMMATION-
VASCULAR CHANGES
IMPORTANT TO BRING ANTIBODIES AND
LEUCOCYTES
1. VASODILATATION
 EARLIEST EVENT
 ARTERIOLES- OPENING OF CAPILLARIES
 INCREASED BLOOD FLOW- RUBOR AND CALOR
2. INCREASED PERMEABILITY
3. STASIS

9. Increased Vascular Permeability (Vascular
Leakage)
 Contraction of endothelial cells resulting in
increased interendothelial spaces is the most
common mechanism of vascular leakage.

10. VASCULAR CHANGES-INCREASED
PERMEABILITY-MECHANISMS
FORMATION OF ENDOTHELIAL GAPS IN
VENULES
 RAPID,SHORT LIVED
 Agent: Histamine,bradykinin
 MECHANISM: Phosphorylation Of Cytoskeletal
Proteins Contraction
 IMMEDIATE TRANSIENT RESPONSE

11. Endothelial injury, resulting in endothelial
cell necrosis and detachment

12. VASCULAR CHANGES-INCREASED
PERMEABILITY-MECHANISMS
DIRECT INJURY
 IMMEDIATE SUSTAINED RESPONSE
 ALL LEVELS
 NECROTIZING INJURIES (e.g.SEVERE BURN)

13. VASCULAR CHANGES-INCREASED
PERMEABILITY-MECHANISMS
DELAYED PROLONGED LEAKAGE
 VENULES,CAPILLARIES
 THERMAL INJURIES,X-RADIATION
 AFTER 2-12 HOURS,LASTS FOR HOURS OR DAYS

14. Neutrophils that adhere to the endothelium during
inflammation may also injure the endothelial cells
and thus amplify the reaction.

15. VASCULAR CHANGES-INCREASED
PERMEABILITY-MECHANISMS
LEUCOCYTE MEDIATED ENDOTHELIAL
INJURY
 DELAYED PROLONGED RESPONSE
 COMMON IN GLOMERULI AND LUNGS

16. VASCULAR CHANGES-INCREASED
PERMEABILITY-MECHANISMS
INCREASED TRANSCYTOSIS
 ACROSS ENDOTHELIAL CYTOPLASM
 INCREASE IN NO: AND SIZE OF TRANSENDOTHELIAL
CHANNELS
LEAKAGE FROM NEW BLOOD VESSELS
 IMPORTANT DURING EARLY PHASES OF HEALING

17. VASCULAR CHANGES-
INCREASED PERMEABILITY
 ESCAPE OF PROTEIN RICH FLUID AND BLOOD
CELLS - FORMATION OF EXUDATE
 TRANSUDATE
 FLUID WITH LOW PROTEIN
 DUE TO OSMOTIC OR HYDROSTATIC IMBALANCE
 VASCULAR PERMEABILITY INTACT

18. Transcytosis:
may involve channels consisting of interconnected, uncoated
vesicles and vacuoles called the vesiculovacuolar organelle:
located close to intercellular junctions.

19. EXUDATE Vs TRANSUDATE
Exudate Transudate
Protein content High Low
Cells & debris High Low
Specific gravity > 1.020 < 1.012
Cause vascular hydrostatic
permeability pressure; 
osmotic pressure
Associated with Inflammation
Exudate Transudate

21. Responses of Lymphatic Vessels
 lymph flow is increased and helps drain edema fluid,
leukocytes, cell debris, as well as microbes.
 Lymphatic vessels also proliferate.
 +/-(lymphangitis),+/-(lymphadenitis).
 Inflamed lymph nodes are often enlarged because of
hyperplasia of the lymphoid follicles and increased
numbers of lymphocytes and macrophages. This
constellation of pathologic changes is termed
reactive, or inflammatory, lymphadenitis

22. summary
 Inflammation-acute and chronic
 Acute - cardinal sign
stimuli
changes -vascular & cellular
•vascular- vasodilation;
increased vascular permeability
transcytosis