1. Acute inflammation 2
By Dr. S. Homathy

2. Mechanism of formation of transudate

3. Starling’s law 'relating to fluid flux between vessels and interstitium

5. ‘Starlg’s law’ relating to fluid flux between vessels and interstitium

6. Mechanism of increased permeability
Endothelial “gaps”- due to endothelial cell contraction
Direct endothelial Injury
Leukocyte mediated Injury
Increased transocytosis (endo/exo)
Leakage from new vessels
Endothelial retraction

8. Endothelial cell contraction leads to intercellular gaps in venules
Reversible process elicited by
Histamines, bradykinins, leukotrienes
cause an early, brief (15 – 30 min.) immediate transient response
in the form of endothelial cell contraction
that widens intercellular gaps of venules (not arterioles, capillaries)

9. Endothelial cell retraction
Cytokine mediators (TNF, IL-1) induce
endothelial cell junction retraction through
cytoskeleton reorganization
4 – 6 hrs post injury,
lasting 24 hrs or more

10. Direct endothelial cell injury causing endothelial cell necrosis and detachment
Severe injuries(burns, infection) may cause
immediate direct endothelial cell damage (necrosis, detachment) making them leaky until they are repaired
immediate sustained response
(immediately after injury and to persist for hours / days until the damaged vessel is repaired)

11. may cause delayed damage as in thermal or UV injury or some bacterial toxins
delayed prolonged leakage
Start 2-12 hours after injury and persist several hours or even days

13. Leukocyte mediated endothelial injury
Marginating and endothelial cell-adherent leukocytes may pile-up
damage the endothelium through
activation and release of toxic oxygen radicals
proteolytic enzymes
(leukocyte-dependent endothelial cell injury) making the vessel leaky
Mosly in venules and pulmonary capilaries
Late response
Long – lived (hour)

14. Increased transcytosis
Certain mediators (VEGF) may cause increased transcytosis
via intracellular vesicles which travel from the luminal to basement membrane surface of the endothelial cell
Usually in venules

15. Leakage from regenerating capillaries
New vessels remain leaky until endothelial cells differentiate sufficiently to form intercellular junction
New endothelial cells also have increased expression of receptors for vasoactive mediators
Directly induce increased vascular permeability via transcytosis.

16. All or any combination of these events may occur in response to a given stimulus

17. Exudate
Tissue oedema
Neutrophil margination …. And emigration

19. This example of edema with inflammation is not trivial at all:
there is marked laryngeal edema such that the airway is narrowed.
This is life-threatening.
fluid collections can be serious depending upon their location.

20. Here is an example of fluid collection into a body cavity, or an effusion.
This is a right pleural effusion (in a baby).
Note the clear, pale yellow appearance of the fluid.
This is a serous effusion.

21. Effusions into body cavities can be further described as follows:
Serous: a transudate with mainly edema fluid and few cells.
Serosanguinous: an effusion with red blood cells.
Fibrinous (serofibrinous): fibrin strands are derived from a protein-rich exudate.
Purulent: numerous PMN's are present.
Also called "empyema" in the pleural space.

22. Pus: A purulent exudate
an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris.

23. Fibrinous pericarditis
strands of stringy pale fibrin between visceral and parietal pericardium.

24. Leukocyte exudation / Leukocyte cellular events
Leukocytes leave the vasculature routinely through the following sequence of events:
Margination and rolling
Adhesion and transmigration/ Diapedesis (trans-migration across the endothelium)

25. Chemotaxis and activation(Migration toward a chemotactic stimuli from the source of tissue injury and become active)
They are then free to participate in:
Phagocytosis and degranulation
Leukocyte-induced tissue injury

26. Leukocyte extravasation and phagocytosis

27. Rolling, adhesion, and transmigration are mediated by
the binding of complementary adhesion molecule on leukocytes and endothelial surfaces

28. Margination (pavementaion) of WBC
Usually circulating cells are swept by laminar flow against the vessels.
In which the red cells are in the center and the WBC are in the periphery
Can interact with the lining endothelial cells