4. COMPONENTS OF ACUTE
INFLAMMATORY RESPONSE
Vascular
1. Transient vasoconstriction of arterioles : It disappears
within 3-5 seconds in mild injuries
2. Active vasodilatation of arterioles-Histamine-mediated
result in (Hyperemia- increased blood in the area)
5. 3-Increased vascular permeability Histamine-mediated ,
result in (Increased fluid & high MW proteins pass
through widened intercellular junctions)
6. - 4. Formation of fluid exudate, from circulation to the interstitial
tissues. Fibrin-rich fluid
- Contains plasma proteins including Ig, C’ and fibrinogen.
- Helps combat the offending agent by diluting it, increase
lymphatic flow and flooding the area with Ig+C’.
9. Cellular response
. Types of cells involved
1st 24 hours- neutrophils
24 48 hours – macrophages, lymphocytes, plasma
cells.
B. Margination of neutrophils
Due to rouleaux formation of red cells and decreases in
plasma.
10. C. Pavementing of neutrophils
Marginated neutrophils adhere to endothelial surface.
D. Emigration of neutrophils
Neutrophils leave blood vessel through intercellular
junction into interstitial tissue (3-10 mins)
11. E. Chemotactic factors
C5a, leukotriene B4, bacterial products
Neutrophils have receptors for these factors
F. Movement of other cells
Macrophages and lymphocytes also mediated by lymphokines
12. Phagocytosis: Involves:
a) Attachment of opsonized particles to the surface of leukocytes.
c) Engulfment by pseudopods encircling the phagocytosed
particles, creating phagosome. Fusion of lysosomal granules
with the phagosome, leading to degranulation
13. c) Killing and degradation bacteria.
Types of bactericidal mechanisms:
1. O2- dependent mechanism O2→superoxide
2. O2- independent mechanisms e.g lysozyme, lactoferrin
14.
15.
16. Components of acute inflammation
Vascular changes Cellular events
Vasodilation: alterations
in vessel caliber
resulting in increased
blood flow
Increased vascular
permeability: permit
plasma proteins to leave
the circulation
Emigration of the leukocytes
from the microcirculation
and accumulation in the
focus of injury
Principal leukocytes in acute
inflammation are
neutrophils
(polymorphonuclear
leukocytes).
17. Inflammation serves to destroy, dilute or isolate the
injurious agent (microbes, toxins) and eliminate the
necrotic cells and tissues.
18. The 5 cardinal signs of inflammation
Color—heat
Rubor—redness
Tumor—swelling
Dolor—pain
Functio laesa—loss of function
19.
20.
21. Redness/ Heat
Increased rate and volume of blood flow into inflamed
area
Swelling
Accumulation of exudate in the tissues
35. Outcome / Sequelae of acute inflammation
Resolution : Return to normal structure and function
Healing by fibrosis/ later fibrous scar
Suppuration / abscess
Chronic inflammation :Persistence of acute inflammation
converts response to a chronic type
36. Effects of acute inflammation
Beneficial effects
1. Dilution of toxin
2. Entry of antibodies
3. Transport of drugs
4. Fibrin formation
5. Delivery of nutrients & oxygen
6. Stimulation of immune response
37. Harmful effects
1. Enzyme digestion of normal tissues
2. Swelling- causing (respiratory) obstruction and raised
(intracranial) pressure
3. Inappropriate inflammatory response eg. Type 1
hypersensitivity reaction
38. Acute inflammation
rapid in onset (seconds
or minutes)
relatively short duration,
lasting for minutes,
several hours, or a few
days
its main characteristics:
the exudation of fluid and
plasma proteins (edema)
the emigration of
leukocytes, predominantly
neutrophils.
is of longer duration
associated histologically
with the presence of
lymphocytes and
macrophages, the
proliferation of blood
vessels, fibrosis, and tissue
necrosis.
Less uniform.
Chronic inflammation
