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Inflammation &
Repair
Hening P. Syahrin
Basic Science and Fundamental of Nursing
Group
Faculty of Nursing Universitas Indonesia
2009

Inflammation
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What to cover







The purpose of inflammation


The Cardinal signs of acute inflammation &
describe the mechanisms involved in
production of these signs
The comparison of hemodynamic & cellular
phases of the inflammatory response
The difference of acute & chronic
inflammation
The types of inflammatory exudates

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What is Inflammation?

is the reaction of vascularized tissue to local injury


is a series of changes in terminal vascular bed, in blood, in
connective tissues to eliminate the offending irritant and
repair the damaged tissue
involves cellular, humoral, chemical & tissue participations
is one of the most important & useful defense mechanism
Without an adequate inflammatory response none of us
would be living; wound would not heal, minor infection
would become overwhelmed
Ironically, it is also one of the most common means
whereby our own tissues are injured; SLE

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Causes
of
Inflammation
Exogenous







Microbiological agents: e.g. viruses bacteria, fungi,


protozoa. Microbial infections are the commonest
causes of inflammation.
Physical agents: trauma, extremes of heat and cold,
irradiation
Chemical agents (toxins): irritants or corrosive
chemical substances, e.g. sulfuric acid, alkalis.
Foreign bodies: sutures
Immunological reactions: hypersensitivity or
autoimmune- mediated inflammation and transplant
rejection

Endogenous

Tissue ischemia such as myocardial infarction or


pulmonary embolism

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The Roles/purposes of
Inflammation
1. To neutralize & destroy invading &
harmful agents
2. To limit the spread of harmful agents to
other tissue
3. To prepare any damaged tissue for repair

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Inflammation may be categorized


into:
1.

2.

Acute; short in duration, lasting less then


2 weeks & involves a discrete set of
events
Chronic; more diffuse, extends over
longer period & may result in the
formation of scar tissue and deformity

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Events in the inflammatory process

(the same regardless the cause)


Increased vascular permeability
 Emigration of leucocytes
 Phagocytosis


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Acute Inflammation
Characterized by a rapid onset & the
resolution of the tissue changes & damage in
a short period
 Changes occurs locally at the site of injury as
well as systemically
 Acute- phase response
 Vascular & cellular responses
 Associated with chemical mediators
 Hemodynamic & White Blood Cells (WBC)
response; inflammatory exudates


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Manifestation
1. Local signs, a classic description by
Celsus named Cardinal signs
(1) Redness/ tumor
(2) Swelling/ rubor
(3) Heat/ calor
(4) Pain/dolor
(5) Loss of function/functio laesa

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Manifestation
General responses
1.

Fever

2.

Leukocytosis

3.

Proliferation of the
phagocyte system

mononuclear

4.

Injury of parenchyma organs.

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Vascular Response







Immediately after injury


Vasoconstriction vasodilation of arterioles & venules
that supply area
Hyperemic response: congested, redness (erythema)
& warmth
Increased capillary permeability, allows fluid escape
into the tissueswelling (edema)
Pain and impaired function is as a result of swelling &
release of chemical mediators
Benefits: dilute toxic&irritating agents and localizing
the spread of infectious agents

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Fluid exudate
Normally the walls of small blood
vessels are freely permeable to water
and crystalloids but relatively
impermeable to plasma proteins. The
formation of protein-rich fluid
exudates is facilitated by separation
of the intercellular junction of the
endothelium.

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The fluid exude carries into the


inflamed area the following important
constituents:

Serum bactericidal factors

a.

Antibodies which act by opsonising


bacteria prior to phagocytosis and by
neutralizing exotoxins

b. Components of the complement


system

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Interferon: a non-specific antiviral agent


Fibrinogen which is converted to fibrin. Fibrin
is important in providing:
a. Cement substance uniting severed tissues
b. Scaffold for repair processes
c. Barrier to the spread of organisms
d. Surface against which phagocytosis of adherent
organisms is enhanced
Therapeutic agents-antibiotics, antiinflammatory drugs, etc.

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Leukocyte exudates and phagocytosis


Leukocytic margination,rolling
Adhesion:by the binding of adhesion
molectures
(selections,
immunoglobulins, intergrins, mucin like
glycoproteins)

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Emigrating
It refers to the process by which motile
white cells migrate out of blood vessels.
emigration is an active, energy-dependent
process.
red blood cell out of blood vessels, called
diapedesis

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White cell transmigration

It is include following
handings:
WBC margination


WBC adhesion with


endothelial surface
adhesion molecule

WBC transmigration
2-12 minute

EM: White cell transmigration

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Chemotaxis
Following
extravasations,
leukocytes
emigrate in tissues toward the site of injury
by a process called chemotaxis.

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Phagocytosis
Recognition and attachment of the
particle to the surface of the
phagocyte engulfment killing
and degradation

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Types of
cells):

leukocyte

(inflammatory

Leukocytes are out of blood vessels that are


known as inflammatory cells.

a. Neutrophils:
Small phagocytic cell
Commonly seen in early stage of
inflammation, and acute inflammation, and
purulent inflammation.

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b. Macrophages:
Tissue macrophages are derived from blood
monocytes that emigrate from blood vessels
under influence of chemotactic factors.
Commonly seen in later stage of inflammation,
chronic
inflammation,
non-purulent
inflammation, and viral, or protozoal, or fungal
infections. And macrophages are also related
to specific immune response.

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c. Eosinophilia
Commonly seen in hypersensitivity
reaction and human parasitological
infections.

d. Lymphocytes and plasma cells


Commonly seen in virus infection and
chronic inflammation.

e. Basophilic and mast cell

MacrM
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3. Proliferation
Proliferate constitution:
Endothelium,
macrophages,
and
fibroblasts commonly seen in later stage
of inflammation

Inflammatory Mediator
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Definition:
It is the chemical substances which
cause or participate in inflammation

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Main mediators function


Functio
n
Vasodilatio
n
Vascular
Leakage

Types of mediator
Histamine, Bradykinin, Nitric oxide,
Prostaglandins PGE2, PGD2,PGF2, PGI2
Histamine, Bradykinin, C3a, C5a, PAF, active oxygen
metabolic products, Leukotrienes C4, D4, E4
Substance P

Chemotaxi C5a, LTB4, bacterial products, IL-8, TNF.


s
Fever
IL-1, IL-6, TNF, PG.
Pain

PGE2, Bradykinin

Tissue
damage

Neutrophil and macrophage lysosomal enzymes


Oxygen metabolites, Nitric oxide

Significances of Inflammation
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1. Significances
( 1 ) Inflammation is fundamentally a
protective response whose ultimate goal
is torid the organism of both the initial
cause of cell injury and the consequences
of such injury, the necrotic cells and
tissues.
(2) Inflammatory response is closely
intertwined with the process of repair.

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(3) The inflammatory response occurs in


the vascularized connective tissue.
(4) Inflammatory response of both
vascular and cellular responses are
mediated by inflammatory mediators
chemical factors derived from plasma
or cells and triggered by the
inflammatory stimulus.
(5) However, inflammatory responses are
not perfect that may be potentially
harmful.

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2. Aspects of inflammation
(1) Many systemic and local host factors
influence
the
adequacy
of
the
inflammatory- reparative response.
Nutrition condition
Immune condition
Endocrine condition
Characteristics of inflammatory organ
or tissue

Tissue Repair &


Wound Healing
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What to cover







Define parenchymal & stromal


Compare labile, stabile, permanent cell
types in terms of their capacity for
regeneration
Describe healing by primary & secondary
intention
Trace the wound healing process
Explain factors affecting wound healing

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Regeneration:
The surviving healthy cells
nearby damage proliferate and
move for repair.

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Type of Regeneration
(1) Complete regeneration:
The new tissue is the same with the
loss in structure and faction.
Commonly
in
physiological
regeneration.

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Conditions:
the ability of regeneration of
parenchymal tissue is strong.
damage area is small and the
stromal framework of the injured
tissue is preservative well.

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The regenerative capacity types


of cells
(1) Labile cells: normally a continuous
process of active replacement is
occurring.
The
chances
of
restoration
by
regeneration are excellent.
Examples: the covering epithelium, the
bone marrow cells and the lymphoid
cells.

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(2) Stable cells:


Although normally the replacement
requirements are minimal, they have not
lost the capacity to proliferate in
response to stimulation. Chances of
regeneration remain.
Examples: adenocytes of parenchymal
viscera (including endocrine); all stromal
elements.

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(3) Permanent cells:


Normally are unable to multiply after
the growth early in life.
Examples: nerve cells, striated and
cardiac muscle cells, smooth muscle
cells.
But peripheral nerve has retained the
capacity for regeneration with damage.

Repair by connective
tissue
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Proliferation of fibroblasts and


capillary buds and the
subsequent laying down of
collagen to produce a scar is the
usual consequence of most
tissue damage.

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1. Definition:
This is young connective tissue,
which is rich in young fibroblasts
and capillaries

2. Morphology
(1) gross feature: pink, soft, moist, and
granular appearance.

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(2) LM:
fibroblasts:
new capillaries: capillary sprout and migrate
toward the wound. The new capillary
endothelial cells are swollen and capillary
tubes are narrow. These new vessels have
leaky interendotheial junctions. Allow the
passage of proteins and red cells into the
extravascular space, thus, new granulation
tissue is often edematous.
inflammatory cells

Provided by prof. Song W.Wong

Granulation tissue

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(Provided by prof. Orr)

Scar tissue

Scar tissue

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Wound Healing
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1. Definition:
Refers to the bodys replacement of
destroyed tissue by living tissue

2. Stages in healing of wound


(1) Escape of blood and exudates
(2) Acute inflammation

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( 3 ) Contraction of the wound. The


causes of contraction are not known but
possible mechanisms are:
Shrinkage of scab in superficial wounds
Contraction properties of granulation
tissue attributable to contraction of
myofibroblasts or tissue re-modeling.

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(4) Proliferation and migration


fibroblasts and endothelial cells.

of

(5) Progressive increase in mature


collagen fibres during the second
week forming a scar.
(6) Loss vascularity and shrinkage of
the scar.

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3. Type of wound healing


(1) Healing by fist intention
A clean wound with a minimum
of space between the margins.

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(2) Healing by second intention


Healing by second intention differs
from healing by first intention in:
Greater tissue loss
More inflammatory exudates and
necrotic material to remove
More granulation tissue therefore a
bigger scar

healing by second intention


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Wound contraction necessary


Slower process
Increased liability to infection
(3) Healing under scab

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4. Factors influencing wound healing


(1) Local factors adversely affecting healing
Type of wounding agent; blunt, crushing,
tearing etc.
Infection
Foreign bodies in wound
Poor blood supply

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Excessive movement
Poor apposition of margins, e. g.
large haematoma formation
Poor wound contraction due to
tissue tethering
Infiltration by tumor.
Previous irradiation.

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(2) General factors adversely affecting


healing
Age
Poor nutrition
 Deficiency of protein
 Lack of Vitamin C results in abnormal
granulation tissue and deficient collagen
production
 Zinc deficiency

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Excessive glucocorticosteroid
production or administration
Fall in temperature

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