Inflammation-1

"Opportunities are usually

disguised by hard work, so
most people don't recognize
them."
- Ann Landers
Shashi-Mar 2000

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INFLAMMATION
dr. Al Munawir, M.Kes., Ph.D.
Laboratorium Patologi Anatomi
Fakultas Kedokteran
Universitas Jember

Shashi-03/08/16

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Introduction:
Inflame to set fire.
Inflammation is dynamic response of
vascularised tissue to injury.
Is a protective response.
Serves to bring defense & healing
mechanisms to the site of injury.
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Lewis Triple Response:

Flush: capillary dilatation.
Flare: arteriolar dilatation.
Weal: exudation, edema.

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Red, Warm & Swollen

(Flare, Flush & Weal Lewis)

Triple response

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Gastric Ulcer:

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Laryngitis:

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Mouth Aphthus ulcer

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Acute Enteritis:

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Pneumonia

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Cardinal Signs of Inflammation

Rubor : Redness Hyperaemia.
Calor : Warm Hyperaemia.
Dolor : Pain Nerve, Chemical med.
Tumor: Swelling Exudation
Loss of Function:

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Inflammation - Mechanism
1. Vaso dilatation
2. Exudation - Edema
3. Emigration of cells
4. Chemotaxis
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Mechanism of Inflammation:

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Neutrophil Margination

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Vascular changes

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Pneumonia - Exudation

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Chemical Mediators:

Chemical substances synthesised or

released which mediate the changes in
inflammation.
Histamine by mast cells - vasodilatation.
Prostaglandins Cause pain & fever.
Bradykinin - Causes pain.

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Morphologic types

Acute:
Exudative

Inflammation: excess fluid. TB lung.

Suppuration/Purulent Bacterial - neutrophils
Fibrinous pneumonia fibrin
Serous excess clear fluid Heart, lung
Haemorrhagic b.v.damage - anthrax.

Chronic inflammation: with healing.

Grannulomatous

clusters of epitheloid* cells

eg. TB, Fungus, Foreign body.
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Never let the competition define you.

Instead, you have to define yourself
based on a point of view you care
deeply about.
Tom Chappel

Shashi-Mar 2000

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Inflammation Outcome
Fibrosis/Scar
Resolution

Injury

Acute
Inflammation

Chronic
Inflammation

Abscess

Fungus
Virus
Cancers
T.B. etc.

Ulcer
Fistula

Sinus
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Chronic Inflammation:

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Edema

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Serous Inflammation - Effusion

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Serous
Inflammation
- Effusion

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Fibrinous
Inflammation

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Purulent - Inflammation - PUS

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Purulent Inflammation PUS

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Purulent Inflammation PUS

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Chronic
Inflammation:
Lung Abscess

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Granuloma:

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Acute Vs Chronic

Flush, Flare &

Weal
Acute
inflammatory cells
- Neutrophils
Vascular damage
More exudation
Little or no fibrosis

Little signs Fibrosis,

Chronic
inflammatory cells
Lymphocytes
Neovascularisation
No/less exudation
Prominent fibrosis
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"People who soar, are those

who refuse to sit back and
wish things would change."
Charles R. Swindoll
Author and Pastor
Shashi-Mar 2000

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The 5 Cardinal Signs of

Heat

Redness Swelling

Pain Loss Of Func.

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Healing & Repair

dr. Al Munawir, M.Kes., Ph.D.
Laboratorium Patologi Anatomi
Fakultas Kedokteran
Universitas Jember

Shashi-03/08/16

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Stages of Healing:

Hemorrhage
Inflammation
Granulation tissue (soft callus)
Scar Fibrosis (hard callus)
Remodeling & Wound strength

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Repair

Regeneration of injured tissue by

parenchymal cells of the same type
Replacement by connective tissue
In other words
Regeneration
Scar

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Proliferative Potential

Labile cells - continuously dividing

Epidermis,

mucosal epithelium, GI tract

epithelium etc

Stable cells - low level of replication

Hepatocytes,

renal tubular epithelium,

pancreatic acini

Permanent cells - never divide

Nerve

cells, cardiac myocytes, skeletal mm

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Polypeptide growth factors

Most Important Mediators affecting Cell

Growth
Present in serum or produced locally
Exert pleiotropic effects; proliferation, cell
migration, differentiation, tissue
remodeling
Regulate growth of cells by controlling
expression of genes that regulate cell
proliferation
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Repair by connective tissue

Occurs when repair by parenchymal
regeneration alone cannot be
accomplished
Involves production of Granulation Tissue
replacement of parenchymal cells with
proliferating fibroblasts and vascular
endothelial cells

Shashi-Mar 2000

Components of the process

of fibrosis

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Angiogenesis - New vessels budding

from old
Fibrosis, consisting of emigration and
proliferation of fibroblasts and deposition
of ECM
Scar remodeling, tightly regulated by
proteases and protease inhibitors
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Wound healing

Induction of acute inflammatory response

by an initial injury
Parenchymal cell regeneration
Migration and proliferation of
parenchymal and connective tissue cells

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Wound healing (contd)

Synthesis of ECM proteins

Remodeling of parenchymal elements to
restore tissue function
Remodeling of connective tissue to
achieve wound strength

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Healing by
First Intention
Focal Disruption of
Basement Membrane
and loss of only a few
epithelial cells
e.g. Surgical Incision

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Healing by
Second Intention
Larger injury, abscess,
infarction
Process is similar but
Results in much larger
Scar and then
CONTRACTION

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Wound Strength

After sutures are removed at one week,

wound strength is only 10% of
unwounded skin (Walker Law)
By 3-4 months, wound strength is about
80% of unwounded skin (Walkers Law)

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Granulation tissue

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Healing
Skin wound

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Healing - Skin Scar

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Factors affecting Healing:

Systemic
Age
Nutrition
Vitamin def.
Immune status
Other diseases

Local
Infection
Size or extent.
apposition
Blood supply
Mobility
Foreign body
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Summary:

Healing Proliferation & Differentiation.

Labile, Stabe & Permanent cells
Stages of Healing: 1-2-3-4.
Healing by First or Second intention.
Skin wound healing - bone healing.
Factors affecting healing Local /
Systemic

Shashi-Mar 2000

"Each time you are honest and conduct

yourself with honesty, a success force will
drive you toward greater success. Each
time you lie, even with a little white lie,
there are strong forces pushing you
toward failure."
Joseph Sugarman
Author and Marketing Specialist