By Dr. Ghada Ahmed

Lecturer of pathology

Benha Faculty of Medicine

Part I Objectives

• 1- Define inflammation• 2- Classify types of inflammation• 3- Explain mechanism of acute inflammation• 4- Enumerate the cardinal signs of acute

inflammation

Definition

• Reaction of living tissue

• Aims to:• 1- prevent tissue damage• 2- localization of irritant• 3- destruction of irritant• 4- preparing for repair

Irritant lymphatic cellularvascular

Irritant (types & effects)

Inflammation

Acute Subac

uteChroni

c

Acute inflammation

Rapid tissue respon

se

Short duratio

n

Mild/ severe irritant

Cardinal signs of inflammation

Mechanism of acute inflammation

Local changes

1- Tissue destruction

2- Vascular phenomenon

3- Rx of tissue histiocytes

1- Local tissue destruction

Injurious agent

Chemical mediators

Local tissue

destruction

2. Local Vascular phenomenon

Transient VC VD Stasis

Inflammatory exudat

e

Dilatation of lymph

atic vessels

Fluid exudate: = inflammatory extravascular fluid

capillary HP cap permeability tissue OP

Exudate Cellularity

Sp gravity

Protein content

(fibrinogen- clot)

Fluid exudate

Function of fluid exudate

• Formation of fibrin network• Dilutes bacterial toxins• Brings antibodies to destruct irritant

N.B: Chemotaxis & Phagocytosis

Inflammatory exudate

Cellular

Margination

Migration

Activation

Diapedesis

Fluid

Cellular exudate

Function of cellular exudate

• PNLs enzymes

attak, phagocytose, kill the organism

• Later : phagocytosis by macrophages

Chemotaxis

Attraction of leucocytes towards the irritant by chemotactic factors

Phagocytosis

Ingestion and destruction of foreign body and bacteria by phagocytic cells

2. Local Vascular phenomenon

Transient VC VD Stasis

Inflammatory exudat

e

Dilatation of lymph

atic vessels

3. Local reaction of tissue hiseocytes

• By macrophages:

• Proliferate • Phagocytosis: dead bacteria, necrotic debris• Clean the area of inflammation

Part II Objectives

• 1- Explain mechanism of acute inflammation• 2- Define chemical mediators and discuss

their role in acute inflammation• 3- Discuss the fate of acute inflammation• 4- Classify then discuss types of acute

inflammation

Mechanism of acute inflammation

Local changes

1- Tissue destruction

2- Vascular phenomenon

3- Rx of tissue histiocytes

Cells of Acute inflammation

PNLs Macrophages

RBCsPus cells

Chemical mediators of acute inflammation

• Chemical factors derived from plasma and cells (e.g. PNLs, monocytes, endoth cs, macrophages, fibroblasts)

• Found as precursors in inactive forms. • Inflammatory stimulus triggers their release,

activation, de novo synthesis

• Act by binding to specific receptors on target cells

Chemical mediators of acute inflammation

• Examples:

• PGs: VD, fever, pain

• Histamine, serotonin: increased permeability

• C5a: increased permeability, chemotaxis

• Cytokines: chemotaxis, leukocyte activation

• Lysosomal enz of PNLs & macrophages: tissue damage

Fate of acute inflammation

Chronicity

Spread Resolution

Quiz • Mark TRUE or FALSE:1- Histamine release causes increased capillary permeability.

2- Diapedesis is an energy-dependent process.

3- Acute inflammation is a rapid tissue response against severe irritants only.

4- Opsonization is covering leucocytes with opsonin to target it for phagocytosis.

Acute inflammation

Suppurative

Localized Diffuse

Non-suppurative

Suppurative inflammation

• Definition:Acute inflammation chch by PUS formation

• Cause: Pyogenic organism (staph, strept,……)

Suppurative inflammation

• Chch of pus

• Composition of pus

Localizes suppurative inflammation(Abscess )

• Definition • Sites • Cause

Pathogenesis of abscess

Pathogenesis of abscess

opening

Cavity containing pus

Pyogenic membrane

Complications of abscess

Chronicity Spread

Complications of healing

Complications of abscess healing

keloid

• Furuncle (boil)

• Carbuncle

Diabetes

Diffuse suppurative inflammation

• Cellulitis

• Definition • Sites• Cause• Differs from abscess….

Complications of diffuse suppurative inflammation

• Acute Lymphangitis• Acute Lymphadenitis• Thrombophlebitis• Septicaemia

Spread

Non-suppurative inflammation

• Types: (according to features of exudate)

1- Catarrhal infl.2- Membranous infl.3- Fibrinous 4- Serous 5- Serofibrinous infl.6- Hemorrhagic7- Necrotizing8- Allergic

Catarrhal inflammation

• Definition:• Sites• Morphology • Fate

Catarrhal inflammation

Membranous (pseudomembranous) inflammation

• Definition • Examples • Pathogenesis• Morphology• Complications

Exotoxin

Membranous (pseudomembranous) inflammation

Part III Objectives

• 1- classify then discuss types of acute inflammation

• 2- define chronic inflammation, its causes, features and types

• 3- compare between acute and chronic inflammation

Non-suppurative inflammation

• Types: (according to features of exudate)

1- Catarrhal infl.2- Membranous infl.3- Fibrinous 4- Serous 5- Serofibrinous infl.6- Hemorrhagic7- Necrotizing8- Allergic

• Fibrinous inflammation

• Serous inflammation

• Serofibrinous inflammation

Serofibrinous inflammation

Serofibrinous inflammation

• Hemorrhagic infl.

Necrotizing infl.

• Allergic infl.

Non-suppurative inflammation

• Types: (according to features of exudate)

1- Catarrhal infl.2- Membranous infl.3- Fibrinous 4- Serous 5- Serofibrinous infl.6- Hemorrhagic7- Necrotizing8- Allergic

Chronic inflammation

Chronic

inflammatio

n

Chronic inflammation

• When????• Persistent infections: – Acute infl. fail to cure– Repeated acute infl.

• Start de novo (T.B.)

• Prolonged exposure to toxic agents

• Autoimmunity

Morphology of chronic inflammations

• Tissue destruction• Blood vessels• Fluid exudate• Cellular exudate

Cells of chronic inflammation

Lymphocytes Esinophils Plasma cells

Giant cells

Fibroblasts

Microscopic picture of chronic inflammation

EAO

Perivascular infiltrate

EAO

Microscopic picture of chronic inflammation (cellular exudate)

Chronic inflammation

Specific(granuloma) Non-specific

Compare between acute & chronic inflammation

Acute chronic

Onset Sudden Gradual

Duration Short Prolonged

Vascular phenomenon

Present Slight/ absent

Cardinal signs Present Slight/ absent

Cells PNLs, pus cs, macrophages

Lymphocytes, plasma cs, macrophages, giant cs, fibroblasts

Bl.vessels Thin, dilated, congested

EAO