Post on 27-May-2015
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Acute Inflammation
ByDr Mohammad Manzoor Mashwani
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.
Time course
Acute inflammation: Less than 48 hours
Chronic inflammation: Greater than 48 hours
(weeks, months, years)
Cell typeAcute inflammation: Neutrophils
Chronic inflammation: Mononuclear cells
(Macrophages, Lymphocytes, Plasma cells).
• Heat • Redness• Swelling• Pain• Loss of function
ACUTE INFLAMMATIONLOCAL MANIFESTATIONS
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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.
Cardinal Signs of Inflammation
Redness : Hyperaemia.
Warm : Hyperaemia.
Pain : Nerve, Chemical
mediators.
Swelling : Exudation
Loss of Function: Pain
MechanismInflammation
1. Vaso dilatation
2. Exudation -
Edema
3. Emigration of
cells
4. Chemotaxis
Major components of Ac. Inflammation
• It has three major components: 1. Alterations in vascular caliber that lead to an
increase in blood flow2. 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.
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Increased Vascular Permeability (Vascular Leakage)
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• 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.
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• Fever• Chills• Myalgia• Malaise
ACUTE INFLAMMATIONSYSTEMIC MANIFESTATIONS
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1. Leukocytosis 2. Increased ESR 3. Elevated serum acute phase proteins
(C-reactive protein, fibrinogen, etc)4. Hypercoagulability
ACUTE INFLAMMATIONLABORATORY MANIFESTATIONS
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STIMULI for acute inflammation
1.1. INFECTIOUSINFECTIOUS2.2. PHYSICALPHYSICAL3.3. CHEMICALCHEMICAL4. Tissue Necrosis5. Foreign Bodies (FBs)6. Immune “responses”, or “complexes”
ACUTE INFLAMMATION• VASCULARVASCULAR EVENTS
• CELLULARCELLULAR EVENTS
• ““MEDIATORS”MEDIATORS”
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
EXUDATION
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• AN EXUDATE: A filtrate of blood plasma.Extravascular fluidHigh protein concentrationContains 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.
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.
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PUSNeutrophils + Dead cells + MicrobesA purulent (infectious) inflammatory
exudate.Rich in leukocytes.Mostly neutrophilsDebris of dead cells & In many cases microbes.
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Leukocyte exudation
Divided into 4 steps
1.1. Margination, rolling, and adhesion to endotheliumMargination, rolling, and adhesion to endothelium
2.2. Diapedesis (trans-migration across the endothelium)Diapedesis (trans-migration across the endothelium)
3.3. Migration toward a chemotactic stimuli from the Migration toward a chemotactic stimuli from the
source of tissue injury.source of tissue injury.
4.4. PhagocytosisPhagocytosis
PHAGOCYTOSIS• RECOGNITION
• ENGULFMENT
• KILLING (DEGRADATION/DIGESTION)
Inflammation Outcome
Acute Inflammation
Resolution
Chronic Inflammation
Abscess
SinusFistula
Fibrosis/Scar
Ulcer
Injury
FungusVirus
CancersT.B. etc.
Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 12 May 2005 10:21 PM)
© 2005 Elsevier
Factors affecting outcome of acute inflammation
1. Severity of tissue damage 2. Capacity of cells to divide3. Type of agent causing damage4. The responsiveness of the
host5. Site involved
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Morphologic PATTERNSof Acute INFLAMMATION
• SerousSerous (watery)
• FibrinousFibrinous (hemorrhagic, rich in FIBRIN)• SuppurativeSuppurative (PUS)
•UlcerativeUlcerative
BLISTER, “Watery”, i.e., SEROUS
PUS
=
PURULENT
ABSCESS
=
OF
PUS
Ulcerative
• Necrotic and eroded epithelial surface• Underlying acute and chronic inflammation• Trauma, toxins, vascular insufficiency
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Summary