2. Definition
• It is a rapid host response that serves to deliver
leukocytes and plasma proteins, such as
antibodies, to sites of infection or tissue injury.
• Minutes- Hours- Days
• Less than 48 hours.
3. Time course
Acute inflammation: Less than 48 hours
Chronic inflammation: Greater than 48 hours
(weeks, months, years)
Cell type
Acute inflammation: Neutrophils
Chronic inflammation: Mononuclear cells
(Macrophages, Lymphocytes, Plasma cells).
5. Pathogenesis: Three main processes occur at the site
of inflammation, due to the release of chemical
mediators :
1.Increased blood flow (redness and warmth).
2.Increased vascular permeability (swelling, pain & loss
of function).
3.Leukocytic Infiltration.
6. Cardinal Signs of Inflammation
Redness : Hyperaemia.
Warm : Hyperaemia.
Pain : Nerve, Chemical
mediators.
Swelling : Exudation
Loss of Function: Pain
10. Major components of Ac.
Inflammation
• It has three major components:
1. Alterations in vascular caliber that lead to an
increase in blood flow
2. Structural changes in the microvasculature that
permit plasma proteins and leukocytes to leave
the circulation.
3. Emigration of the leukocytes from the
microcirculation, their accumulation in the
focus of injury, and their activation to eliminate
the offending agent.
10
11. Increased Vascular Permeability
(Vascular Leakage)
• A hallmark of acute inflammation causing edema.
• Contraction of endothelial cells resulting in increased
interendothelial spaces is elicited by chemical mediators.
• It is immediate transient response usually short-lived (15–30
minutes).
• In some mild injuries e.g burns, x or ultraviolet radiation, certain
bacterial toxins, occurs after a delay of 2 to 12 hours lasting for
several hours or days, mild endothelial damage.
• Late-appearing sunburn is an example of this type of leakage.
• Increased transport of fluids and proteins, called transcytosis,
through the endothelial cell.
11
17. :Lymphatics in inflammation
Lymphatics are responsible for draining edema.
Edema: An excess of fluid in the interstitial tissue
or serous cavities; either a transudate or an
exudate
18. EXUDATION
• AN EXUDATE: A filtrate of blood plasma.
Extravascular fluid
High protein concentration
Contains cellular debris &
High specific gravity.
• Its presence implies an increase in the normal
permeability of small blood vessels in an area of
injury and, therefore, an inflammatory reaction.18
19. TRANSUDATE:
A fluid with low protein content
Little or no cellular material &
Low specific gravity.
It is an ultrafiltrate of plasma, resulting from
osmotic or hydrostatic imbalance across the vessel
wall without an increase in vascular permeability.
19
20.
21. PUS
Neutrophils + Dead cells + Microbes
A purulent (infectious) inflammatory
exudate.
Rich in leukocytes.
Mostly neutrophils
Debris of dead cells &
In many cases microbes.
21
22. Leukocyte exudation
Divided into 4 steps
1. Margination, rolling, and adhesion to endothelium
2. Diapedesis (trans-migration across the endothelium)
3. Migration toward a chemotactic stimuli from the
source of tissue injury.
4. Phagocytosis
27. Factors affecting outcome of acute
inflammation
1. Severity of tissue damage
2. Capacity of cells to divide
3. Type of agent causing damage
4. The responsiveness of the host
5. Site involved
27
28. Morphologic PATTERNS
of Acute INFLAMMATION
• Serous (watery)
• Fibrinous (hemorrhagic, rich
in FIBRIN)
• Suppurative (PUS)
• Ulcerative
The usual suspects, again. “Stimuli”, like “etiologic agents” is a very elusive term if you like to think in terms of ultimate causes.
These are the three “phases”, in order, of acute inflammation. Please NOTE they, in no way, are the independent of each other, and as you might suspect by now, quite the contrary, CRUCIALLY all wrapped up with each other!
The three phases of phagocytosis, in correct order.
I must have said THREE patterns, but this looks like four to me. Who cares? Remember, they are only adjectives! (Onelook.com has 133 adjectives to the word “inflammation”)