acute inflammation by dr mohammad manzoor mashwani

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Acute Inflammation By Dr Mohammad Manzoor Mashwani

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Page 1: Acute inflammation by Dr Mohammad Manzoor Mashwani

Acute Inflammation

ByDr Mohammad Manzoor Mashwani

Page 2: Acute inflammation by Dr 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.

Page 3: Acute inflammation by Dr Mohammad Manzoor Mashwani

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).

Page 4: Acute inflammation by Dr Mohammad Manzoor Mashwani

• Heat • Redness• Swelling• Pain• Loss of function

ACUTE INFLAMMATIONLOCAL MANIFESTATIONS

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Page 5: Acute inflammation by Dr Mohammad Manzoor Mashwani

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.

Page 6: Acute inflammation by Dr Mohammad Manzoor Mashwani

Cardinal Signs of Inflammation

Redness : Hyperaemia.

Warm : Hyperaemia.

Pain : Nerve, Chemical

mediators.

Swelling : Exudation

Loss of Function: Pain

Page 7: Acute inflammation by Dr Mohammad Manzoor Mashwani
Page 8: Acute inflammation by Dr Mohammad Manzoor Mashwani
Page 9: Acute inflammation by Dr Mohammad Manzoor Mashwani

MechanismInflammation

1. Vaso dilatation

2. Exudation -

Edema

3. Emigration of

cells

4. Chemotaxis

Page 10: Acute inflammation by Dr Mohammad Manzoor Mashwani

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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Page 11: Acute inflammation by Dr Mohammad Manzoor Mashwani

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.

Page 12: Acute inflammation by Dr Mohammad Manzoor Mashwani

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Page 13: Acute inflammation by Dr Mohammad Manzoor Mashwani

• Fever• Chills• Myalgia• Malaise

ACUTE INFLAMMATIONSYSTEMIC MANIFESTATIONS

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Page 14: Acute inflammation by Dr Mohammad Manzoor Mashwani

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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Page 15: Acute inflammation by Dr Mohammad Manzoor Mashwani

STIMULI for acute inflammation

1.1. INFECTIOUSINFECTIOUS2.2. PHYSICALPHYSICAL3.3. CHEMICALCHEMICAL4. Tissue Necrosis5. Foreign Bodies (FBs)6. Immune “responses”, or “complexes”

Page 16: Acute inflammation by Dr Mohammad Manzoor Mashwani

ACUTE INFLAMMATION• VASCULARVASCULAR EVENTS

• CELLULARCELLULAR EVENTS

• ““MEDIATORS”MEDIATORS”

Page 17: Acute inflammation by Dr Mohammad Manzoor Mashwani

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

Page 18: Acute inflammation by Dr Mohammad Manzoor Mashwani

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.

Page 19: Acute inflammation by Dr Mohammad Manzoor Mashwani

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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Page 20: Acute inflammation by Dr Mohammad Manzoor Mashwani
Page 21: Acute inflammation by Dr Mohammad Manzoor Mashwani

PUSNeutrophils + Dead cells + MicrobesA purulent (infectious) inflammatory

exudate.Rich in leukocytes.Mostly neutrophilsDebris of dead cells & In many cases microbes.

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Page 22: Acute inflammation by Dr Mohammad Manzoor Mashwani

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

Page 23: Acute inflammation by Dr Mohammad Manzoor Mashwani
Page 24: Acute inflammation by Dr Mohammad Manzoor Mashwani

PHAGOCYTOSIS• RECOGNITION

• ENGULFMENT

• KILLING (DEGRADATION/DIGESTION)

Page 25: Acute inflammation by Dr Mohammad Manzoor Mashwani

Inflammation Outcome

Acute Inflammation

Resolution

Chronic Inflammation

Abscess

SinusFistula

Fibrosis/Scar

Ulcer

Injury

FungusVirus

CancersT.B. etc.

Page 26: Acute inflammation by Dr Mohammad Manzoor Mashwani

Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 12 May 2005 10:21 PM)

© 2005 Elsevier

Page 27: Acute inflammation by Dr Mohammad Manzoor Mashwani

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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Page 28: Acute inflammation by Dr Mohammad Manzoor Mashwani

Morphologic PATTERNSof Acute INFLAMMATION

• SerousSerous (watery)

• FibrinousFibrinous (hemorrhagic, rich in FIBRIN)• SuppurativeSuppurative (PUS)

•UlcerativeUlcerative

Page 29: Acute inflammation by Dr Mohammad Manzoor Mashwani

BLISTER, “Watery”, i.e., SEROUS

Page 30: Acute inflammation by Dr Mohammad Manzoor Mashwani

PUS

=

PURULENT

ABSCESS

=

POCKET

OF

PUS

Page 31: Acute inflammation by Dr Mohammad Manzoor Mashwani

Ulcerative

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

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Summary