By
Dr. Ghada Ahmed
Lecturer of pathology
Benha Faculty of
Medicine
Part I Objectives
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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
vascular
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•
•
•
•
lymphatic
cellular
Aims to:
1- prevent tissue damage
2- localization of irritant
3- destruction of irritant
4- preparing for repair
Irritant
Irritant (types & effects)
Inflammation
Acute
Subacute
Chronic
Short
duration
Mild/
severe
irritant
Rapid
tissue
response
Acute inflammation
Cardinal signs of inflammation
Mechanism of acute inflammation
Local
changes
1- Tissue
destruction
General
changes
1- changes in blood cells
2- fever
3- loss of appetite
2- Vascular
phenomenon
3- Rx of
tissue
histiocytes
4- liver secretes proteins
5-hyperplasia of draining
LN
6- degenerative changes
7- septicemia
8- pyemia
1- Local tissue destruction
Injurious
agent
Local
tissue
destruction
Chemical
mediators
2. Local Vascular
phenomenon
Transient
VC
VD
Stasis
Inflammat
ory
exudate
Dilatation
of
lymphatic
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
Inflammatory
exudate
Cellular
Margination
Fluid
Migration
N.B: Chemotaxis
Activation
&
Phagocytosis
Diapedesis
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
Inflammat
ory
exudate
Dilatation
of
lymphatic
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
General
changes
1- changes in blood cells
2- fever
3- loss of appetite
2- Vascular
phenomenon
3- Rx of
tissue
histiocytes
4- liver secretes proteins
5-hyperplasia of draining
LN
6- degenerative changes
7- septicemia
8- pyemia
Cells of Acute inflammation
PNLs
Pus cells
Macrophages
RBCs
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
Resolution
Spread
Chronicity
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
Nonsuppurative
Suppurative
Localized
Diffuse
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
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Definition
Sites
Cause
Differs from abscess….
Complications of diffuse suppurative
inflammation
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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- Hemorrhagic
7- Necrotizing
8- Allergic
Catarrhal inflammation
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•
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•
Definition:
Sites
Morphology
Fate
Catarrhal inflammation
Membranous (pseudomembranous)
inflammation
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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- Hemorrhagic
7- Necrotizing
8- 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- Hemorrhagic
7- Necrotizing
8- Allergic
Chronic
inflammation
Prolonged
duration
Attempts of
healing
Chronic
inflamma
tion
Tissue
destruction
Active
inflammation
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
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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
EAO
Perivascular infiltrate
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
Cardinal signs
Present
Slight/ absent
Present
Slight/ absent
Cells
PNLs, pus cs,
macrophages
Bl.vessels
Thin, dilated,
congested
Lymphocytes,
plasma cs,
macrophages, giant
cs, fibroblasts
EAO