acute inflammation by dr mohammad manzoor mashwani

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

=

POCKET

OF

PUS

Ulcerative

• Necrotic and eroded epithelial surface• Underlying acute and chronic inflammation• Trauma, toxins, vascular insufficiency

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Summary