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CONTENTS
2.1: Definitions & Concepts Of Inflammation
2.2: Stages Of Inflammation
2.3: Mediators Of Inflammation
2.4: Morphologic Pattern Of Acute & Chronic
Inflammation
2.5: Repair Or Healing
2
2.1: Definitions & Concepts Of
Inflammation
• The local response of living mammalian
tissues to injury due to any agent.
• Body defense reaction in order to eliminate or
limit the spread of injurious agent as well as to
remove the consequent necrosed cells and
tissues.
3
• Causes of inflammation;
i. Physical agent e.g. mechanical trauma, radiation
etc.
ii. Chemical agent e.g. simple chemical poisons,
organic poisons
iii. Infective agents e.g. bacteria, viruses, parasites,
their toxins
iv. Immunological agents e.g. Ag-Ab reaction, cell
mediated
4
• Involves 2 basic
processes (overlapping):
• Have protective role
against injurious agents
• Cause considerable
harm to the body
eg; anaphylaxis,
atherosclerosis etc
5
Inflammatory
response
healing
Signs of Inflammation
• The famous 4 cardinal signs of inflammation:
(i) rubor (redness)
(ii) tumor (swelling)
(iii) calor (heat)
(iv) dolor (pain)
Added latest – functio laesa (loss of function)
6
2.2: Stages Of Inflammation
INFLAMMATION
ACUTE
INFLAMMATION
CHRONIC
INFLAMMATION
7
8
9
10
11
12
5-hydro-peroxy –icosa-tetra-enoic acid (5-HPETE)
13
• Acute inflammation
– Short duration & represents the early body
reaction and usually followed by repair
– The main features :
(a) Accumulation of fluid & plasma at the
affected site
(b) Intravascular activation of platelets
(c) Polymorphonuclear neutrophils as
inflammatory cells
14
• Chronic Inflammation
- longer duration and occurs either :
(a) after the causative agent of acute
inflammation persists for a long
time
(b) Stimulus that induces chronic
inflammation from the beginning
- main features :
presence of chronic inflammatory cells
(lymphocytes, plasma cells and
macrophages)
I) ACUTE INFLAMMATION
• The changes can be conveniently described
under:
(i) Vascular events
(ii) Cellular events
17
Infected toenail showing the characteristic redness and
swelling associated with acute inflammation
(i) VASCULAR EVENTS
• Alteration in the microvasculature (arterioles,
capillaries & venules)
• Earliest response to tissue injury
• Alterations includes:
(a) haemodynamic changes
(b) changes in vascular permeability
18
(a) Haemodynamic Changes
• Earliest features of inflammatory response
result from changes in the vascular flow and
calibre of small blood vessels in the injured
tissue
19
The sequence of these changes:
20
Transient vasoconstriction
Persistent progressive vasodilatation
Local hydrostatic pressure
Slowing or stasis
Leucocytic margination
• Lewis Triple Response/ red line response;
(Eg: form stroking with a blunt point)
i. Red line : Appears a few second;
Capillary & venules dilatation
ii. Flare : Bright reddish
appearance/flush surrounding
the red line; Anteriolar dilation
iii. Wheal : Swelling or oedema of the
surrounding skin occurring due
to transudation of fluid into the
extravascular space 21
22
Triple response
(b) Altered vascular permeability
• Vascular changes begin quickly after the injury
but may develop at variables rates, depending on
the nature & severity of the original injury.
• The interchange of fluid between the vascular &
extra vascular space results from balance of fluid
into the vascular space or out into the tissues;
i. Hydrostatic pressure
ii. Oncotic pressure - protein
iii. Osmotic pressure
iv. Lymph flow
23
Fluid interchange between blood and
extracellular fluid (ECF). (HP = Hydrostatic
pressure, OP = Osmotic pressure)
24
NO
OEDEMA OEDEMA
Edema
25
• MECHANISMS OF INCREASED VASCULAR
PERMEABILITY
(i) Endothelial cell contraction
(ii) Endothelial cell retraction
(iii)Direct injury to endothelial cells
(iv)Endothelial injury mediated by leucocytes
(v) Neovascularisation
27
a) Contraction of endothelial cells
• Microvasculature : venules
• Response type :
Immediate transient (15-30 min)
• Pathogenesis :
Histamine, bradykinin, other chemical
mediators
• Examples : Mild thermal injury
28
b) Retraction of endothelial cells
• Microvasculature : venules
• Response type :
somewhat delayed (in 4 – 6 hrs)
prolonged (for 24 hrs or more)
• Pathogenesis :
Interleukin-1(IL-1)
Tumor Necrosis Factor (TNF)
• Examples : In vitro experimental work only
29
c) Direct injury to endothelial cells
• Microvasculature : Arteriols, venules,
capillaries
• Response type :
Immediate sustained leakage (immediate after
injury prolonged (hrs to days)
Delayed sustained leakage (delayed (2-12hrs)
prolonged (hrs-days))
30
• Pathogenesis :
cell necrosis and detachment
• Examples : Moderate to severe burns, severe
bacterial infection, radiation injury
31
d) Endothelial injury mediated by
leucocytes
• Microvasculature : venules, capillaries
• Response type :
delayed, prolonged
• Pathogenesis :
Leucocyte activation
• Examples : pulmonary venules and capillaries
32
e) Neovascularisation
• Microvasculature : All levels
• Response type :
Any type
• Pathogenesis :
Angiogenesis, vascular endothelial growth
factor (VEGF)
• Examples : Healing, tumors
33
ii) CELLULAR EVENTS
• Cellular events; cells of the acute inflammatory
response are the neutrophils, monocytes &
macrophages.
Polymorphonuclear neutrophils (PMNs)
(within 24 hrs; Life long 24-48 hrs)
Monocytes
Macrophages
(24-48 hrs; Survive much longer) 34
• The movements of neutrophils out of the vessels
& their role in combat can be divided into 5
steps;
i. Margination = ?
ii. Adhesion = ?
iii. Emigration/ diapedesis=?
iv. Chemotaxis = ?
v. Phagocytosis & degranulation=?
35
• Concentrates the leucocytes adjacent to endothelial
wall- Margination
• Adherence of inflammatory cell to the endothelium/
vascular basement membrane- Adhesion
• Neutrophil lodged between endothelial cell and
basement membrane and escape out into the
extravascular space- Diapedesis
• Chemotactic factor mediated transmigration of
leucocytes to reach the interstitial tissue- Chemotaxis
• The process of engulfment of solid particulate
material bt the cell (cell eating)- Phagocytosis
36
THE INFLAMMATION PROCESS
37
38
Neutrophil Margination
39
FATE OF ACUTE INFLAMMATION
• Acute inflammation generally has one of FOUR
(4) outcomes;
i. Resolution – complete return to normal/ tissue
changes are slight and cellular changes are
reversible eg; resolution in lobar pneumonia
ii. Healing by scarrimg– tissue destruction is
extensive, no tissue regeneration; healing by
fibrosis
40
iii) Suppuration – the progression process of
severe necrosis cause by pyogenic bacteria;
neutrophilic infiltration; form an abcess;
abcess – organised by dense fibrous tissue
and get calcified
iv) Progression to chronic inflammation may
follow acute inflammation, although signs
of chronic inflammation may be present at
the onset of injury; healing proceed side by
side.
41
An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of
necrotic tissue surround central areas of pus
42
II) CHRONIC INFLAMMATION
• Chronic inflammation;
prolonged process in which tissue
destruction and inflammation occur
at the same time.
43
• Caused one of the following 3 ways:
i) Chronic inflammation following acute
inflammation – the tissue destruction is
extensive, or bacteria survive & persist in
small numbers at the site of acute
inflammation
ii) Recurrent attacks of acute inflammation –
repeated bouts of acute inflammation eg;
repeated acute infection of gallbladder
chronic cholecystitis
iii) Starting de novo – infection with organisms
of low pathogenecity (chronic from the
beginning) 44
• General features of Chronic inflammation:
i. Infiltration with mononuclear cells
Infiltrated by mononuclear inflammatory cells :
phagocytes & lymphoid cells
phagocytes : circulating monocytes, tissue
macrophages, epithelioid cells, multinucleated
giants cells
ii. Tissue destruction
Central feature of lesions
iii. Proliferative changes
Result of necrosis, proliferation of small vessels
and fibroblasts; healing by fibrosis and collagen
45
Systemic effects of chronic
inflammation
Associated with following systemic features:
1. Fever – mild fever, loss of weight and
weakness
2. Anemia – varying degree of anemia
3. Leucocytosis - general
4. ESR – elevated in all cases
5. Amyloidosis – long term cases of chronic
suppurative inflammation (secondary
systemic (AA) amyloidosis 46
Types of chronic inflammation
NON-SPECIFIC
• Formation of granulation
tissue and healing by
fibrosis
• Eg; Chronic osteomyelitis,
Chronic ulcer
SPECIFIC
• Injurious agent causes a
characteristic histologic
tissue response
• Eg; tuberculosis, leprosy,
syphilis
47
Types of chronic inflammation (based
on histological classification)
CHRONIC NON-SPECIFIC
INFLAMMATION
• Characterised by:
(a) non-specific
inflammatory cell
infiltration eg; chronic
osteomyelitis, lung abcess
(b) Infiltration by
polymorphs and abcess
formation Eg; Actinomycosis
CHRONIC GRANULOMATOUS
INFLAMMATION
• Formation of granulomas
• Eg; tuberculosis, leprosy,
syphilis, sarcoidosis
48
Granulomatous Inflammation
• Granulomatous inflammation; mechanism whereby the
body deals with certain “indigestible” bacteria, fungi, or
foreign particles.
• Examples;
i. Bacteria e.g. Tuberculosis, Leprosy
ii. Parasitic e.g. Schistosomiasis
iii. Fungal e.g. Blastomycosis, Histoplasma capsulatum
iv. Inorganic metals or dusts e.g. Silicosis
v. Foreign body e.g. Vascular graft
vi. Unknown e.g. Sarcoidosis
49
50
INJURY
(e.g; by M. tuberculosis, talc
Failure to digest agent
Weak acute inflammatory response
Persistence of injurious agent
T cell-mediated immune response Poorly digestible agent
•Activation of CD+4 T cells (release of
lymphokines IL-1, IL-2. growth factors
IFN-ˠ and IFN-ɑ)
•Monocyte chemotactic factor
51
Accumulation of tissue macrophages
(Increased recruitment from circulation, local proliferation)
Macrophages activated by IFN-ˠ
Transformed to epithelioid cells, giant cells
GRANULOMA
Granuloma tissue
52
• Examples of disorders associated with inflammation
include;
i. Asthma
ii. Autoimmune diseases
iii. Hypersensitivities
iv. Pelvic inflammatory disease
v. Rheumatoid arthritis
vi. Transplant rejection
53
2.3: Mediators Of Inflammation
• What are mediators?
i. May be circulating in the plasma or may be produced
locally by cells at the site of inflammation.
ii. Induce their effects by binding to specific reactors on
target cells.
iii. May stimulate target cells to release secondary effector
molecules.
iv. May act on only one or a very few targets.
v. Function is generally tightly regulated.
54
• 2 types of chemical mediators of Acute inflammation;
i. Plasma-derived mediators e.g. kinin system,
coagulation & fibrinolytic system, complement
system.
ii. Cell-derived mediators e.g. vasoactive amines,
cytokines, platelet activating factor, growth factor.
55
• Chronic inflammatory cells & mediators;
i. Macrophages
ii. T & B-lymphocytes
iii. Eosinophils
iv. Mast cells
56
• Inflammatory cells release mediators such as;
i. Cytokines-
(IL-8, interferon-neutrophil)
ii. Vasoactive amines-
(histamine, serotinin- mast cell, basophil, platelet)
iii. Prostanoids-
(arachidonic acid metabolics)
iv. Reactive oxygen intermediates-
(released from activated neutrophil)
57
• If the mediators in the inflammatory response are
successful;
i. Invading & infectious agents will be removed.
ii. Damaged tissues will be disposed of.
iii. New tissue will be induced to form.
iv. New blood supply to the area will be established.
58
Chronic Inflammation – Lung Abscess
59
2.4: Morphologic Patterns Of Acute & Chronic
Inflammation
• Serous inflammation; excessive clear watery
fluid with a variable protein content but no
fibrin e.g. pleural effusion associated with
tuberculosis.
60
Serous Inflammation - effusion
61
Serous Inflammation - effusion
62
• Fibrinous inflammation; the formation of
fibrin is striking e.g. in acute pleurisy.
63
Fibrinous Inflammation
64
• Purulent (Suppurative) inflammation;
production of pus is the main characteristic
e.g. abscess & acute apendicitis.
65
Purulent Inflammation - PUS
66
• Ulceration; complication of many disease
process
• Divided into 2 groups;
i. Simple ulcer
ii. Malignant (cancerous) ulcer
67
A skin ulcer resulting from infection with Corynebacterium
diphtheriae
68
Mouth Apthus Ulcer
69
Gastric Ulcer
70
2.5: Repair Or Healing
• The processes that take place during & after
the injury are;
i. Removal of dead & foreign material.
ii. Regeneration of injured tissue from cells
of the same type.
iii. Replacement of damage tissue by new
connective tissue.
71
• Cells can be divided into 3 major groups;
i. Labile (continuous dividing) e.g. epithelial &
blood cells.
ii. Stable (low level of replication; decrease or lose
their ability to proliferate after adolescence) e.g.
fibroblast, smooth muscle cells, bone & cartilage
cells
iii. Permanent (never divide) e.g. nerve cells, cardiac
myocytes.
72
HEALING
• 2 processes:
(i) Granulation tissue formation
(ii) Contraction of wounds
73
(i) Granulation tissue formation
• 3 phases :
(a) PHASE OF INFLAMMATION
trauma, blood clots (site of injury)
acute response :exudation of plasma,
neutrophils, monocytes (24 hours)
74
(b) PHASE OF CLEARANCE
- proteolytic enzymes from neutrophils
- Autolytic enzymes from dead tissue
cells
- Phagocytic activity : macrophages
(function : clear of the necrotic tissue,
debris & RBCs)
75
(c) PHASE OF INGROWTH OF GRANULATION
2 main processes:
i. Angiogenesis (neovascularisation)
formation of new blood vessels
ii. Fibrogenesis
formation of fibrocytes and mitotic
division by fibroblasts; myofibroblasts
In 6th days, more collagen is formed
76
ii) Contraction of wounds
• Start after 2 -3 days; completed: 14th day
• Wound reduced 80% of its original size
• Contraction occur: rapid healing process
• Factors under mechanism of wound
contraction:
(a) dehydration
(b) contraction of collagen
(c) myofibroblasts
77
WOUND HEALING
1. Healing by first intention (Primary union)
characteristics:
- clean & uninfected
- surgical incised
- without much loss of cells & tissue
- edges of wound – surgical sutures
78
2. Healing by second intention (Secondary
union)
Characteristics:
- Large tissue defect
- extensive loss of cells & tissues
- not approximated by surgical sutures but
left open
79
• 5 stages of healing (primary Union);
i. Initial Haemorrhage
ii. Acute Inflammation response
iii. Epithelial changes
iv. Organization
v. Suture tracks
80
• 6 stages of healing (secondary Union);
i. Initial Hemorrhage
ii. Inflammation phase
iii. Epithelial changes
iv. Granulation tissue
v. Wound contraction
vi. Presence of infection
81
• Repair; regeneration of injured tissue by
parenchymal cells of the same type.
• Replacement by connective tissue occur when
repair by parenchymal regeneration alone cannot
be accomplished.
• Involves production of Granulation tissue.
• Replacement of parenchymal cells with
proliferating fibroblasts & vascular endothelial
cells.
82
Scars present on the skin, evidence of fibrosis &
healing of a wound
83
Granulation tissue
84
Healing Skin wound
85
Healing - Skin scar
86
• Factors affecting healing;
i. Systemic e.g. age, nutrition, immune
status.
ii. Local e.g. infection, blood supply,
mobility, foreign body.
87

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inflammation

  • 1. 1
  • 2. CONTENTS 2.1: Definitions & Concepts Of Inflammation 2.2: Stages Of Inflammation 2.3: Mediators Of Inflammation 2.4: Morphologic Pattern Of Acute & Chronic Inflammation 2.5: Repair Or Healing 2
  • 3. 2.1: Definitions & Concepts Of Inflammation • The local response of living mammalian tissues to injury due to any agent. • Body defense reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cells and tissues. 3
  • 4. • Causes of inflammation; i. Physical agent e.g. mechanical trauma, radiation etc. ii. Chemical agent e.g. simple chemical poisons, organic poisons iii. Infective agents e.g. bacteria, viruses, parasites, their toxins iv. Immunological agents e.g. Ag-Ab reaction, cell mediated 4
  • 5. • Involves 2 basic processes (overlapping): • Have protective role against injurious agents • Cause considerable harm to the body eg; anaphylaxis, atherosclerosis etc 5 Inflammatory response healing
  • 6. Signs of Inflammation • The famous 4 cardinal signs of inflammation: (i) rubor (redness) (ii) tumor (swelling) (iii) calor (heat) (iv) dolor (pain) Added latest – functio laesa (loss of function) 6
  • 7. 2.2: Stages Of Inflammation INFLAMMATION ACUTE INFLAMMATION CHRONIC INFLAMMATION 7
  • 8. 8
  • 9. 9
  • 10. 10
  • 11. 11
  • 13. 13
  • 14. • Acute inflammation – Short duration & represents the early body reaction and usually followed by repair – The main features : (a) Accumulation of fluid & plasma at the affected site (b) Intravascular activation of platelets (c) Polymorphonuclear neutrophils as inflammatory cells 14
  • 15. • Chronic Inflammation - longer duration and occurs either : (a) after the causative agent of acute inflammation persists for a long time (b) Stimulus that induces chronic inflammation from the beginning - main features : presence of chronic inflammatory cells (lymphocytes, plasma cells and macrophages)
  • 16. I) ACUTE INFLAMMATION • The changes can be conveniently described under: (i) Vascular events (ii) Cellular events 17 Infected toenail showing the characteristic redness and swelling associated with acute inflammation
  • 17. (i) VASCULAR EVENTS • Alteration in the microvasculature (arterioles, capillaries & venules) • Earliest response to tissue injury • Alterations includes: (a) haemodynamic changes (b) changes in vascular permeability 18
  • 18. (a) Haemodynamic Changes • Earliest features of inflammatory response result from changes in the vascular flow and calibre of small blood vessels in the injured tissue 19
  • 19. The sequence of these changes: 20 Transient vasoconstriction Persistent progressive vasodilatation Local hydrostatic pressure Slowing or stasis Leucocytic margination
  • 20. • Lewis Triple Response/ red line response; (Eg: form stroking with a blunt point) i. Red line : Appears a few second; Capillary & venules dilatation ii. Flare : Bright reddish appearance/flush surrounding the red line; Anteriolar dilation iii. Wheal : Swelling or oedema of the surrounding skin occurring due to transudation of fluid into the extravascular space 21
  • 22. (b) Altered vascular permeability • Vascular changes begin quickly after the injury but may develop at variables rates, depending on the nature & severity of the original injury. • The interchange of fluid between the vascular & extra vascular space results from balance of fluid into the vascular space or out into the tissues; i. Hydrostatic pressure ii. Oncotic pressure - protein iii. Osmotic pressure iv. Lymph flow 23
  • 23. Fluid interchange between blood and extracellular fluid (ECF). (HP = Hydrostatic pressure, OP = Osmotic pressure) 24 NO OEDEMA OEDEMA
  • 25. • MECHANISMS OF INCREASED VASCULAR PERMEABILITY (i) Endothelial cell contraction (ii) Endothelial cell retraction (iii)Direct injury to endothelial cells (iv)Endothelial injury mediated by leucocytes (v) Neovascularisation 27
  • 26. a) Contraction of endothelial cells • Microvasculature : venules • Response type : Immediate transient (15-30 min) • Pathogenesis : Histamine, bradykinin, other chemical mediators • Examples : Mild thermal injury 28
  • 27. b) Retraction of endothelial cells • Microvasculature : venules • Response type : somewhat delayed (in 4 – 6 hrs) prolonged (for 24 hrs or more) • Pathogenesis : Interleukin-1(IL-1) Tumor Necrosis Factor (TNF) • Examples : In vitro experimental work only 29
  • 28. c) Direct injury to endothelial cells • Microvasculature : Arteriols, venules, capillaries • Response type : Immediate sustained leakage (immediate after injury prolonged (hrs to days) Delayed sustained leakage (delayed (2-12hrs) prolonged (hrs-days)) 30
  • 29. • Pathogenesis : cell necrosis and detachment • Examples : Moderate to severe burns, severe bacterial infection, radiation injury 31
  • 30. d) Endothelial injury mediated by leucocytes • Microvasculature : venules, capillaries • Response type : delayed, prolonged • Pathogenesis : Leucocyte activation • Examples : pulmonary venules and capillaries 32
  • 31. e) Neovascularisation • Microvasculature : All levels • Response type : Any type • Pathogenesis : Angiogenesis, vascular endothelial growth factor (VEGF) • Examples : Healing, tumors 33
  • 32. ii) CELLULAR EVENTS • Cellular events; cells of the acute inflammatory response are the neutrophils, monocytes & macrophages. Polymorphonuclear neutrophils (PMNs) (within 24 hrs; Life long 24-48 hrs) Monocytes Macrophages (24-48 hrs; Survive much longer) 34
  • 33. • The movements of neutrophils out of the vessels & their role in combat can be divided into 5 steps; i. Margination = ? ii. Adhesion = ? iii. Emigration/ diapedesis=? iv. Chemotaxis = ? v. Phagocytosis & degranulation=? 35
  • 34. • Concentrates the leucocytes adjacent to endothelial wall- Margination • Adherence of inflammatory cell to the endothelium/ vascular basement membrane- Adhesion • Neutrophil lodged between endothelial cell and basement membrane and escape out into the extravascular space- Diapedesis • Chemotactic factor mediated transmigration of leucocytes to reach the interstitial tissue- Chemotaxis • The process of engulfment of solid particulate material bt the cell (cell eating)- Phagocytosis 36
  • 36. 38
  • 38. FATE OF ACUTE INFLAMMATION • Acute inflammation generally has one of FOUR (4) outcomes; i. Resolution – complete return to normal/ tissue changes are slight and cellular changes are reversible eg; resolution in lobar pneumonia ii. Healing by scarrimg– tissue destruction is extensive, no tissue regeneration; healing by fibrosis 40
  • 39. iii) Suppuration – the progression process of severe necrosis cause by pyogenic bacteria; neutrophilic infiltration; form an abcess; abcess – organised by dense fibrous tissue and get calcified iv) Progression to chronic inflammation may follow acute inflammation, although signs of chronic inflammation may be present at the onset of injury; healing proceed side by side. 41
  • 40. An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of necrotic tissue surround central areas of pus 42
  • 41. II) CHRONIC INFLAMMATION • Chronic inflammation; prolonged process in which tissue destruction and inflammation occur at the same time. 43
  • 42. • Caused one of the following 3 ways: i) Chronic inflammation following acute inflammation – the tissue destruction is extensive, or bacteria survive & persist in small numbers at the site of acute inflammation ii) Recurrent attacks of acute inflammation – repeated bouts of acute inflammation eg; repeated acute infection of gallbladder chronic cholecystitis iii) Starting de novo – infection with organisms of low pathogenecity (chronic from the beginning) 44
  • 43. • General features of Chronic inflammation: i. Infiltration with mononuclear cells Infiltrated by mononuclear inflammatory cells : phagocytes & lymphoid cells phagocytes : circulating monocytes, tissue macrophages, epithelioid cells, multinucleated giants cells ii. Tissue destruction Central feature of lesions iii. Proliferative changes Result of necrosis, proliferation of small vessels and fibroblasts; healing by fibrosis and collagen 45
  • 44. Systemic effects of chronic inflammation Associated with following systemic features: 1. Fever – mild fever, loss of weight and weakness 2. Anemia – varying degree of anemia 3. Leucocytosis - general 4. ESR – elevated in all cases 5. Amyloidosis – long term cases of chronic suppurative inflammation (secondary systemic (AA) amyloidosis 46
  • 45. Types of chronic inflammation NON-SPECIFIC • Formation of granulation tissue and healing by fibrosis • Eg; Chronic osteomyelitis, Chronic ulcer SPECIFIC • Injurious agent causes a characteristic histologic tissue response • Eg; tuberculosis, leprosy, syphilis 47
  • 46. Types of chronic inflammation (based on histological classification) CHRONIC NON-SPECIFIC INFLAMMATION • Characterised by: (a) non-specific inflammatory cell infiltration eg; chronic osteomyelitis, lung abcess (b) Infiltration by polymorphs and abcess formation Eg; Actinomycosis CHRONIC GRANULOMATOUS INFLAMMATION • Formation of granulomas • Eg; tuberculosis, leprosy, syphilis, sarcoidosis 48
  • 47. Granulomatous Inflammation • Granulomatous inflammation; mechanism whereby the body deals with certain “indigestible” bacteria, fungi, or foreign particles. • Examples; i. Bacteria e.g. Tuberculosis, Leprosy ii. Parasitic e.g. Schistosomiasis iii. Fungal e.g. Blastomycosis, Histoplasma capsulatum iv. Inorganic metals or dusts e.g. Silicosis v. Foreign body e.g. Vascular graft vi. Unknown e.g. Sarcoidosis 49
  • 48. 50 INJURY (e.g; by M. tuberculosis, talc Failure to digest agent Weak acute inflammatory response Persistence of injurious agent T cell-mediated immune response Poorly digestible agent •Activation of CD+4 T cells (release of lymphokines IL-1, IL-2. growth factors IFN-ˠ and IFN-ɑ) •Monocyte chemotactic factor
  • 49. 51 Accumulation of tissue macrophages (Increased recruitment from circulation, local proliferation) Macrophages activated by IFN-ˠ Transformed to epithelioid cells, giant cells GRANULOMA
  • 51. • Examples of disorders associated with inflammation include; i. Asthma ii. Autoimmune diseases iii. Hypersensitivities iv. Pelvic inflammatory disease v. Rheumatoid arthritis vi. Transplant rejection 53
  • 52. 2.3: Mediators Of Inflammation • What are mediators? i. May be circulating in the plasma or may be produced locally by cells at the site of inflammation. ii. Induce their effects by binding to specific reactors on target cells. iii. May stimulate target cells to release secondary effector molecules. iv. May act on only one or a very few targets. v. Function is generally tightly regulated. 54
  • 53. • 2 types of chemical mediators of Acute inflammation; i. Plasma-derived mediators e.g. kinin system, coagulation & fibrinolytic system, complement system. ii. Cell-derived mediators e.g. vasoactive amines, cytokines, platelet activating factor, growth factor. 55
  • 54. • Chronic inflammatory cells & mediators; i. Macrophages ii. T & B-lymphocytes iii. Eosinophils iv. Mast cells 56
  • 55. • Inflammatory cells release mediators such as; i. Cytokines- (IL-8, interferon-neutrophil) ii. Vasoactive amines- (histamine, serotinin- mast cell, basophil, platelet) iii. Prostanoids- (arachidonic acid metabolics) iv. Reactive oxygen intermediates- (released from activated neutrophil) 57
  • 56. • If the mediators in the inflammatory response are successful; i. Invading & infectious agents will be removed. ii. Damaged tissues will be disposed of. iii. New tissue will be induced to form. iv. New blood supply to the area will be established. 58
  • 57. Chronic Inflammation – Lung Abscess 59
  • 58. 2.4: Morphologic Patterns Of Acute & Chronic Inflammation • Serous inflammation; excessive clear watery fluid with a variable protein content but no fibrin e.g. pleural effusion associated with tuberculosis. 60
  • 59. Serous Inflammation - effusion 61
  • 60. Serous Inflammation - effusion 62
  • 61. • Fibrinous inflammation; the formation of fibrin is striking e.g. in acute pleurisy. 63
  • 63. • Purulent (Suppurative) inflammation; production of pus is the main characteristic e.g. abscess & acute apendicitis. 65
  • 65. • Ulceration; complication of many disease process • Divided into 2 groups; i. Simple ulcer ii. Malignant (cancerous) ulcer 67
  • 66. A skin ulcer resulting from infection with Corynebacterium diphtheriae 68
  • 69. 2.5: Repair Or Healing • The processes that take place during & after the injury are; i. Removal of dead & foreign material. ii. Regeneration of injured tissue from cells of the same type. iii. Replacement of damage tissue by new connective tissue. 71
  • 70. • Cells can be divided into 3 major groups; i. Labile (continuous dividing) e.g. epithelial & blood cells. ii. Stable (low level of replication; decrease or lose their ability to proliferate after adolescence) e.g. fibroblast, smooth muscle cells, bone & cartilage cells iii. Permanent (never divide) e.g. nerve cells, cardiac myocytes. 72
  • 71. HEALING • 2 processes: (i) Granulation tissue formation (ii) Contraction of wounds 73
  • 72. (i) Granulation tissue formation • 3 phases : (a) PHASE OF INFLAMMATION trauma, blood clots (site of injury) acute response :exudation of plasma, neutrophils, monocytes (24 hours) 74
  • 73. (b) PHASE OF CLEARANCE - proteolytic enzymes from neutrophils - Autolytic enzymes from dead tissue cells - Phagocytic activity : macrophages (function : clear of the necrotic tissue, debris & RBCs) 75
  • 74. (c) PHASE OF INGROWTH OF GRANULATION 2 main processes: i. Angiogenesis (neovascularisation) formation of new blood vessels ii. Fibrogenesis formation of fibrocytes and mitotic division by fibroblasts; myofibroblasts In 6th days, more collagen is formed 76
  • 75. ii) Contraction of wounds • Start after 2 -3 days; completed: 14th day • Wound reduced 80% of its original size • Contraction occur: rapid healing process • Factors under mechanism of wound contraction: (a) dehydration (b) contraction of collagen (c) myofibroblasts 77
  • 76. WOUND HEALING 1. Healing by first intention (Primary union) characteristics: - clean & uninfected - surgical incised - without much loss of cells & tissue - edges of wound – surgical sutures 78
  • 77. 2. Healing by second intention (Secondary union) Characteristics: - Large tissue defect - extensive loss of cells & tissues - not approximated by surgical sutures but left open 79
  • 78. • 5 stages of healing (primary Union); i. Initial Haemorrhage ii. Acute Inflammation response iii. Epithelial changes iv. Organization v. Suture tracks 80
  • 79. • 6 stages of healing (secondary Union); i. Initial Hemorrhage ii. Inflammation phase iii. Epithelial changes iv. Granulation tissue v. Wound contraction vi. Presence of infection 81
  • 80. • Repair; regeneration of injured tissue by parenchymal cells of the same type. • Replacement by connective tissue occur when repair by parenchymal regeneration alone cannot be accomplished. • Involves production of Granulation tissue. • Replacement of parenchymal cells with proliferating fibroblasts & vascular endothelial cells. 82
  • 81. Scars present on the skin, evidence of fibrosis & healing of a wound 83
  • 84. Healing - Skin scar 86
  • 85. • Factors affecting healing; i. Systemic e.g. age, nutrition, immune status. ii. Local e.g. infection, blood supply, mobility, foreign body. 87