A topic of General Pathology made easy for third year and M.Phil. students.

1. ACUTE INFLAMMATION
Dr. Sobia Khalid

3. The steps of the inflammatory response can be
remem bered as the five Rs:
• (1) recognition of the injurious agent,
• (2) recruitment of leukocytes
• (3) removal ofthe agent
• (4) regulation (control) of the response
• (5) resolution (repair).

5. CAUSES OF INFLAMMATION
• Infection
• Tissue necrosis
• Foreign bodies
• Immune reactions (also called
hypersensitivity)

6. RECOGNITION OF MICROBES AND
DAMAGED CELLS

7. CELLULAR RECEPTORS FOR MICROBES.
• TLRs
• The receptors are expressed on many cell
types, including epithelial cells, dendritic cells,
macrophages, and other leukocytes.

8. SENSORS OF CELL DAMAGE.
• Uric acid (a product of DNA breakdown),
• ATP (released from damaged mitochondria),
• Reduced intracellular K+ concentrations
(reflecting loss of ions because of plasma
membrane injury),
• DNA when it is released into the cytoplasm
and not sequestered in nuclei.

9. • These receptors induces the production of the
cytokine interleukin1 (IL1).
• IL1 recruits leukocytes and thus induces
inflammation.

10. Other cellular receptors involved in
inflammation.
• Many leukocytes express receptors for the Fc tails
of antibodies and for complement proteins.
• These receptors recognize microbes coated with
antibodies and complement
• (the coating process is called opsonization) and
promote ingestion and destruction of the
microbes as well as inflammation.

11. Circulating proteins.
• A circulating protein called mannose-binding
lectin recognizes microbial sugars and
promotes ingestion of the microbes and the
activation of the complement system.
• Other proteins called collectins also bind to
and combat microbes.

12. ACUTE INFLAMMATION

13. (1) Dilation of small vessels increase in blood
flow
(2) Increased permeability of the
microvasculature plasma proteins and
leukocytes to leave the circulation
(3) Emigration of the leukocytes from the
microcirculation focus of injury and their
activation to eliminate the offending agent.

15. EXUDATE TRANSUDATE
An extravascular fluid that has a high
protein concentration
A fluid with low protein content (most of
which is albumin)
Contains cellular debris Little or no cellular material
An increase in the permeability of small
blood vessels
No increase in vascular permeability
High specific gravity Low specific gravity
It is not an ultra filtrate of blood plasma It is an ultra filtrate of blood plasma
It is produced as a result of tissue injury
and an ongoing inflammatory reaction.
It is produced as a result of osmotic or
hydrostatic imbalance across the vessel
wall.

16. REACTIONS OF BLOOD VESSELS IN
ACUTE INFLAMMATION
• Changes in Vascular Flow and Caliber
• Increased Vascular Permeability (Vascular
Leakage)
• Responses of Lymphatic Vessels and Lymph
Nodes

17. Changes in Vascular Flow and Caliber
• Vasodilation by histamine, on vascular smooth
muscle.
• Increased permeability of the
microvasculature.
• Engorgement of small vessels with slowly
moving red cells…..STASIS.
• Blood leukocytes, principally neutrophils,
accumulate along the vascular endothelium.

18. Increased
Vascular
Permeabi
lity
(Vascular
Leakage)

19. Responses of Lymphatic Vessels and
Lymph Nodes
• In inflammation, lymph flow is increased and
helps drain edema fluid that accumulates.
• Lymphangitis
• Lymphadenitis