6. inflammation

Prepared by: Prof. Mirza
Anwar Baig (AIKTC-SOP)
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6. INFLAMMATION
(Nonspecific Host Defenses)
Presented by: Prof.Mirza Anwar Baig
Anjuman-I-Islam's Kalsekar Technical Campus
School of Pharmacy,New Pavel,Navi
Mumbai,Maharashtra

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Contents:
1. Introduction to inflammation
2. Process/stages of inflammation
a. Vasodilation
b. Phagocytosis
c. Tissue repair and scare formation
3. Acute and chronic inflammation

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Topic learning outcomes:
At the end of you should be able to
1.Describe the functions and features of the
inflammatory response and process of phagocytosis
and tissue repair
2.Differentiation between acute and chronic inflammation.
3.Identify the principle mediators of inflammation and
pharmacotherapeutic targets for its treatment.

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InflammationInflammation
Triggered by tissue damage due toTriggered by tissue damage due to
infection, heat, wound, etc.infection, heat, wound, etc.
Four Major Symptoms of Inflammation:Four Major Symptoms of Inflammation:
1. Redness1. Redness
2. Pain2. Pain
3. Heat3. Heat
4. Swelling4. Swelling
May also observe:May also observe:
5. Loss of function5. Loss of function

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Functions of Inflammation
1.1. Destroy and remove pathogens
2. If destruction is not possible, to limit effects by
confining the pathogen and its products.
3. Repair and replace tissue damaged by pathogen and
its products.

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Table 17.17

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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.

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Stages of Inflammation:
1. Vasodilation: Increase in diameter of blood vessels.
Triggered by chemicals released by damaged cells:
histamine, kinins, prostaglandins, and leukotrienes.
2. Phagocyte Migration and Margination:
Margination is the process in which phagocytes stick
to lining of blood vessels.
Diapedesis (Emigration): Phagocytes squeeze between
endothelial cells of blood vessels and enter
surrounding tissue.
Phagocytes are attracted to site of infection through
chemotaxis.
Phagocytes destroy microbes, as well as dead and
damaged host cells.
3. Tissue Repair: Dead and damaged cells are replaced.

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Process of Inflammation

Phagocytes are Attracted to Site of
Infection by Chemotaxis

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Phagocytosis:
– Derived from the Greek words “Eat and cell”.
– Phagocytosis is carried out by white blood cells:
macrophages, neutrophils, and occasionally
eosinophils.
– Neutrophils predominate early in infection.
– Wandering macrophages: Originate from monocytes
that leave blood and enter infected tissue, and
develop into phagocytic cells.
– Fixed Macrophages (Histiocytes): Located in liver,
nervous system, lungs, lymph nodes, bone marrow,
and several other tissues.

Phagocytic Cells: Macrophages (Monocytes), Neutrophils, and
Eosinophils
(Macrophages)

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PHAGOCYTOSIS

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Stages of Phagocytosis
1. Chemotaxis: Phagocytes are chemically attracted to
site of infection.
2. Adherence: Phagocyte plasma membrane attaches
to surface of pathogen or foreign material.
• Adherence can be inhibited by capsules (S.
pneumoniae) or M protein (S. pyogenes).
• Opsonization: Coating process with opsonins
that facilitates attachment.
–Opsonins include antibodies and complement
proteins.

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Stages of Phagocytosis (Continued)
3.Ingestion: Plasma membrane of phagocytes extends
projections (pseudopods) which engulf the microbe.
Microbe is enclosed in a sac called phagosome.
4.Digestion: Inside the cell, phagosome fuses with
lysosome to form a phagolysosome.
Lysosomal enzymes kill most bacteria within 30
minutes and include:
• Lysozyme: Destroys cell wall peptidoglycan
• Lipases and Proteases
• RNAses and DNAses
After digestion, residual body with undigestable
material is discharged.

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Platelets Form Blood Clots

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• Wound healing (Tissue Repair)
Factors affecting wound healing...
1. Systemic factors:
These include good nutritional status and general health.
Infection, impaired immunity, poor blood supply and
systemic conditions, e.g. diabetes mellitus and cancer,
reduce the rate of wound healing.
2. Local factors: Local factors that facilitate wound
healing include:
• good blood supply providing oxygen and nutrients
and removing waste products
• freedom from contamination by, e.g., microbes,
foreign bodies, toxic chemicals.

24J. Price 24
Acute Inflammation
Elicitation
is Removed
Elicitation is
Persistant or
Reocurring
Normal Wound Healing
Chronic Inflammation
Episodic Acute Inflammation
Nonorganized granulation tissue
Granulomatous inflammation Aberant Wound Healing
genetic or
environmental
interference
Small lesions
Larger tissue deficits
Outcomes

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TISSUE REPAIR

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Characterstics Primary Healing Secondary Healing
Nature of
tissue
destruction
Damaged edges of a wound are
in close apposition.
Blood clot and cell debris fill the
gap
Edges of a wound cannot
be brought into
apposition
Inflammation
Phagocytes begin to remove the
clot and cell debris
Fibroblasts secrete collagen fibres
which begin to bind
the surfaces together.
Phagocytes separates
necrotic tissue (slough)
from the inflammatory
exudate.
Fibroblast: same as PH.
Proliferation
The clot above the new tissue
becomes the scab and sepa-
rates after 3 to 10 days.
Granulation tissue develops,
invading the clot and restoring
the blood supply to the
wound.
Fibroblasts continue to secrete
collagen
This begins with
activation of granulation
tissue.
Some fibroblasts in the
wound develop a
limited ability to contract,
reducing the size of the
wound and healing time.

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Characterstics Primary Healing Secondary Healing
Maturation
Strenthing:
Due to rearrangement
of collagen fibres and
the strength of the
wound increases.
Scare formation:
The granulation tissue
is replaced by fib-
rous scar tissue and
becomes less vascular.
Strenthing:
Same as primary
healing
Scare formation:
The fibrous scar tissue
is shiny and does not
contain sweat glands,
hair follicles or
sebaceous glands
Time required for
healing
Appearing after a few
months as a fine line.
Usually takes over
several months to
restore full thickness of
the skin.

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Table 5–1. Differences between Acute and Chronic Inflammation.
Acute Chronic
Duration Short (days) Long (weeks to months)
Onset Acute Insidious
Specificity Nonspecific Specific (where immune
response is activated)
Inflammatory
cells
Neutrophils, macrophages Lymphocytes, plasma
cells, macrophages,
fibroblasts
Vascular changes Active vasodilation,
increased permeability
New vessel formation
(granulation tissue)
Fluid exudation
and edema
+ –
Cardinal clinical
signs (redness,
heat, swelling,
pain)
+ –

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Acute Chronic
Tissue necrosis
– (Usually)
+ (Suppurative and
necrotizing inflammation)
+ (ongoing)
Fibrosis (collagen
deposition)
– +
Operative host
responses
Plasma factors: complement,
immunoglobulins, properdin,
etc; neutrophils, nonimmune
phagocytosis
Immune response,
phagocytosis, repair
Systemic
manifestations
Fever, often high
Low–grade fever,
weight loss, anemia
Changes in
peripheral blood
Neutrophil leukocytosis;
lymphocytosis (in viral
infections)
Frequently none;
variable leukocyte
changes, increased
plasma
immunoglobulin

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