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INFLAMMATION
1
 Inflammation is part of the complex biological
response of body tissues to harmful stimuli,
such as pathogens, damaged cells or irritants
 The function of inflammation is to eliminate the
initial cause of cell injury, clear out necrotic
cells and tissues damaged from the original
insult and the inflammatory process, and
initiate tissue repair.
2
Cardinal signs
 The traditional names for signs of inflammation
come from Latin:
 Dolor (pain)
 Calor (heat)
 Rubor (redness)
 Tumor (swelling)
 Functio laesa (loss of function)
 Redness and heat are due to increased blood
flow at body core temperature to the inflamed
site
 Swelling is caused by accumulation of fluid
3
Stimuli for Acute Inflammation
• Infections (bacterial, viral, fungal, parasitic) &
microbial toxins
• Tissue necrosis: ischemia, trauma, physical
or
chemical injury (e.g., thermal injury;
irradiation; some environmental chemicals)
• Foreign bodies (splinters, dirt, sutures)
• Immune reactions (aka hypersensitivity
reactions)
4
Acute inflammation
 Main components:
– Vascular changes
• Vasodilation
• Vascular permeability
• Increased adhesion of white blood cells
– Cellular events
• Cellular recruitment and activation of
neutrophils (polymorphonuclear
leukocytes)
5
Aetiology
 Microbial infections: bacterial, viral, fungal,
etc.
 Physical agents: burns, trauma--like cuts,
radiation
 Chemicals: drugs, toxins, or caustic
substances like battery acid.
 Immunologic reactions: rheumatoid
arthritis.
6
7
Acute inflammation
 Time course
 Acute inflammation: Less than 48 hours
 Chronic inflammation: Greater than 48 hours
(weeks, months, years)
 Cell type
 Acute inflammation: Neutrophils
 Chronic inflammation: Mononuclear cells
(Macrophages, Lymphocytes, Plasma cells)
8
Mechanism of Inflammation
1. Vasodilatation
2. Exudation - Edema
3. Emigration of cells
4. Chemotaxis
9
Mechanism of Inflammation
 The major local
manifestations of acute
inflammation
(1) Vascular dilation and
increased blood flow
(causing erythema and
warmth).
(2) Extravasation and
deposition of plasma fluid
and proteins (oedema).
(3) Leukocyte emigration and
accumulation in the site of
injury.
10
Changes in vascular flow
(hemodynamic changes)
 Slowing of the circulation
 outpouring of albumin rich fluid into the
extravascular tissues results in the
concentration of RBCs in small vessels and
increased viscosity of blood.
 Leukocyte margination
 Neutrophils become oriented at the periphery
of vessels and start to stick.
11
 An ultrafiltrate of
blood plasma
 permeability of
endothelium is
usually normal.
 low protein content
( mostly albumin)
 A filtrate of blood
plasma mixed with
inflammatory cells
and cellular debris.
 permeability of
endothelium is
usually altered
 high protein
content.
Transudate Exudate
12
Pus:
A purulent exudate: an inflammatory exudate rich in
leukocytes (mostly neutrophils) and parenchymal cell
debris.
Leukocyte exudation
 Divided into 4 steps
 Margination, rolling, and adhesion to
endothelium
 Diapedesis (trans-migration across the
endothelium)
 Migration toward a chemotactic stimuli from the
source of tissue injury
 Phagocytosis
13
14
Chemical Mediators
Chemical substances synthesised or released and
mediate the changes in inflammation.
 Histamine by mast cells - vasodilatation
 Prostaglandins - Cause pain & fever
 Bradykinin - Causes pain
15
Acute inflammation has one of four
outcomes:
 Abscess formation
 Progression to chronic inflammation
 Resolution- tissue goes back to normal
 Repair- healing by scarring or fibrosis
16
Abscess formation
 "A localised collection of pus (suppurative
inflammation) appearing in an acute or chronic
infection, and associated with tissue destruction,
and swelling.
17
Carbuncle
 It is an extensive form of abscess in which pus is
present in multiple loci and opens at the surface
by sinuses.
 Occurs in the back of the neck and the scalp.
 Furuncle or boil
 It is a small abscess related to hair follicles or
sebaceous glands
 Could be multiple furunclosis
18
19
Cellulitis
 It is an acute diffuse suppurative inflammation
caused by streptococci, which secrete
hyaluronidase & streptokinase enzymes that
dissolve the ground substances and facilitate the
spread of infection.
 Sites:
 Areolar tissue: orbit, pelvis, etc
 Lax subcutaneous tissue
20
21
Examples of disorders
associated with inflammation
 Acne vulgaris
 Asthma
 Autoimmune diseases
 Autoinflammatory diseases
 Celiac disease
 Chronic prostatitis
 Colitis
 Diverticulitis
 Glomerulonephritis
22
Examples of disorders
associated with inflammation
 Hypersensitivities
 Inflammatory bowel diseases
 Otitis
 Pelvic inflammatory disease
 Rheumatic fever
 Rheumatoid arthritis
 Rhinitis
 Sarcoidosis
 Transplant rejection
 Vasculitis
23
24
Acute dermatitis
Acute tonsillitis
Scars present on the skin, evidence of fibrosis and healing of a wound

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Inflammation Mechanisms & Effects

  • 2.  Inflammation is part of the complex biological response of body tissues to harmful stimuli, such as pathogens, damaged cells or irritants  The function of inflammation is to eliminate the initial cause of cell injury, clear out necrotic cells and tissues damaged from the original insult and the inflammatory process, and initiate tissue repair. 2
  • 3. Cardinal signs  The traditional names for signs of inflammation come from Latin:  Dolor (pain)  Calor (heat)  Rubor (redness)  Tumor (swelling)  Functio laesa (loss of function)  Redness and heat are due to increased blood flow at body core temperature to the inflamed site  Swelling is caused by accumulation of fluid 3
  • 4. Stimuli for Acute Inflammation • Infections (bacterial, viral, fungal, parasitic) & microbial toxins • Tissue necrosis: ischemia, trauma, physical or chemical injury (e.g., thermal injury; irradiation; some environmental chemicals) • Foreign bodies (splinters, dirt, sutures) • Immune reactions (aka hypersensitivity reactions) 4
  • 5. Acute inflammation  Main components: – Vascular changes • Vasodilation • Vascular permeability • Increased adhesion of white blood cells – Cellular events • Cellular recruitment and activation of neutrophils (polymorphonuclear leukocytes) 5
  • 6. Aetiology  Microbial infections: bacterial, viral, fungal, etc.  Physical agents: burns, trauma--like cuts, radiation  Chemicals: drugs, toxins, or caustic substances like battery acid.  Immunologic reactions: rheumatoid arthritis. 6
  • 7. 7
  • 8. Acute inflammation  Time course  Acute inflammation: Less than 48 hours  Chronic inflammation: Greater than 48 hours (weeks, months, years)  Cell type  Acute inflammation: Neutrophils  Chronic inflammation: Mononuclear cells (Macrophages, Lymphocytes, Plasma cells) 8
  • 9. Mechanism of Inflammation 1. Vasodilatation 2. Exudation - Edema 3. Emigration of cells 4. Chemotaxis 9
  • 10. Mechanism of Inflammation  The major local manifestations of acute inflammation (1) Vascular dilation and increased blood flow (causing erythema and warmth). (2) Extravasation and deposition of plasma fluid and proteins (oedema). (3) Leukocyte emigration and accumulation in the site of injury. 10
  • 11. Changes in vascular flow (hemodynamic changes)  Slowing of the circulation  outpouring of albumin rich fluid into the extravascular tissues results in the concentration of RBCs in small vessels and increased viscosity of blood.  Leukocyte margination  Neutrophils become oriented at the periphery of vessels and start to stick. 11
  • 12.  An ultrafiltrate of blood plasma  permeability of endothelium is usually normal.  low protein content ( mostly albumin)  A filtrate of blood plasma mixed with inflammatory cells and cellular debris.  permeability of endothelium is usually altered  high protein content. Transudate Exudate 12 Pus: A purulent exudate: an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris.
  • 13. Leukocyte exudation  Divided into 4 steps  Margination, rolling, and adhesion to endothelium  Diapedesis (trans-migration across the endothelium)  Migration toward a chemotactic stimuli from the source of tissue injury  Phagocytosis 13
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  • 15. Chemical Mediators Chemical substances synthesised or released and mediate the changes in inflammation.  Histamine by mast cells - vasodilatation  Prostaglandins - Cause pain & fever  Bradykinin - Causes pain 15
  • 16. Acute inflammation has one of four outcomes:  Abscess formation  Progression to chronic inflammation  Resolution- tissue goes back to normal  Repair- healing by scarring or fibrosis 16
  • 17. Abscess formation  "A localised collection of pus (suppurative inflammation) appearing in an acute or chronic infection, and associated with tissue destruction, and swelling. 17
  • 18. Carbuncle  It is an extensive form of abscess in which pus is present in multiple loci and opens at the surface by sinuses.  Occurs in the back of the neck and the scalp.  Furuncle or boil  It is a small abscess related to hair follicles or sebaceous glands  Could be multiple furunclosis 18
  • 19. 19
  • 20. Cellulitis  It is an acute diffuse suppurative inflammation caused by streptococci, which secrete hyaluronidase & streptokinase enzymes that dissolve the ground substances and facilitate the spread of infection.  Sites:  Areolar tissue: orbit, pelvis, etc  Lax subcutaneous tissue 20
  • 21. 21
  • 22. Examples of disorders associated with inflammation  Acne vulgaris  Asthma  Autoimmune diseases  Autoinflammatory diseases  Celiac disease  Chronic prostatitis  Colitis  Diverticulitis  Glomerulonephritis 22
  • 23. Examples of disorders associated with inflammation  Hypersensitivities  Inflammatory bowel diseases  Otitis  Pelvic inflammatory disease  Rheumatic fever  Rheumatoid arthritis  Rhinitis  Sarcoidosis  Transplant rejection  Vasculitis 23
  • 24. 24 Acute dermatitis Acute tonsillitis Scars present on the skin, evidence of fibrosis and healing of a wound