1. The document discusses inflammation, describing it as the body's protective response to injury or infection that helps rid the body of damaging stimuli and initiate repair of tissues. 2. It notes the four cardinal signs of inflammation as heat, redness, swelling, and pain, and explains the causes, types, and components of the inflammatory response. 3. The summary outlines the functions of inflammation in destroying pathogens, limiting their spread, and repairing damaged tissues, as well as the roles of plasma proteins, leukocytes, and tissue phagocytes in mounting an inflammatory response.

1. By
Dr Mohammad Manzoor
Mashwani

2.  What is inflammation?
 Causes
 Signs
 Types
 Components
 Functions of inflammation
 Overview of inflammation
 Specific host defences
 Summary
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4.  “Inflame” means to “set a fire”
 It is a dynamic response of vascularized tissue to
injury.
 Fundamentally a protective response.
 To rid the organism of both the initial cause of cell
injury like microbes and toxins and the
consequences of such injury e.g necrotic cells and
tissues.
 The survival of organisms depends on their ability
to get rid of damaged or necrotic tissues and
foreign invaders, such as microbes.
 The host response that accomplishes these goals is
called inflammation.
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5.  Inflammation to a specific tissue is denoted by the
suffix " ITIS ", following the name of the tissue:
 Example: Appendicitis, cholecystitis, pulpitis and
gingivitis.
 Pneumonia .

6.  If no inflammation
 Infections go unchecked
 Wounds would never heal
 Injured tissues might remain permanent sores.
 In the practice of medicine the importance of
inflammation is that it can sometimes be
inappropriately triggered or poorly controlled,
and is thus the cause of tissue injury in many
disorders.
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7. a. Infections (viral,bacteral,parasitic)
b. Trauma (blunt, penetrating)
c. Physical & chemical agents
d. Tissue necrosis
e. Foreign bodies (dirt, sutures)
f. Immune reactions (hypersensitivity
reactions)
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8. Four cardinal signs
1. Callor (heat)
2. Rubor (Redness)
3. Tumor (Swelling)
4. Dolor (Pain)
May also obser ve:
5. Loss of function
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9. Cardinal Signs of Inflammation
Calor Rubor Tumor Dolor Loss of Function
first described by Celsus more than 2000 years ago.

10.  Chronological  Morphological
pattern pattern
1. Acute inflammation 1. Serous inflammation
2. Chronic inflammation 2. Suppurative
inflammation
3. Fibrinous inflammation
4. Ulcer
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11. Time view
1. acute (days)
2. subacute (weeks)
3. chronic (months-years)

12. 1. Connective tissue cells
2. Connective tissue matrix
3. Vessels
4. Soluble proteins
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13. 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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14.  Inflammation is a complex reaction of responses of blood
vessels and leukocytes.
 Principal defenders are:
1. Plasma proteins
2. Leukocytes &
3. Tissue phagocytes derived from circulation.
 Being in blood they can home any site where they may be
needed.
 As invaders such as microbes and necrotic cells are
typically present in tissues, outside the circulation, it
follows that the circulating cells and proteins have to be
rapidly recruited to these extravascular sites.
 The inflammatory response coordinates to achieve this
goal.
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15.  Inflammator y response
repair
 It destroys, dilutes, and walls of f the
injurious agent, series of events that tr y
to heal the damaged tissue.
 Repair begins during inflammation but
reaches completion usually af ter the
injurious influence has been
neutralized.
 In the process of repair the injured
tissue is replaced through regeneration
of native parenchymal cells, by filling of
the defect with fibrous tissue (scarring)
or, most commonly, by a combination of 15

16.  Inflammation may be harmful in some
situations.
 When inappropriately directed against self tissues or is
not adequately controlled, it becomes the cause of injury
and disease.
 Inflammatory reactions underlie common chronic
diseases, such as rheumatoid arthritis, atherosclerosis,
and lung fibrosis, as well as life-threatening
hypersensitivity reactions to insect bites, drugs, and
toxins.
 Anti-inflammatory drugs, control the harmful sequelae
of inflammation yet not interfere with its beneficial
effects.
 Inflammation may contribute to a variety of diseases that
are not thought to be primarily due to abnormal host
responses.
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17. Host
Defenses
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18. Introduction
Resistance: Ability to ward off (prevent)
disease.
1. Nonspecific Resistance: Defenses that protect
against all pathogens.
2. Specific Resistance: Protection against
specific pathogens.
Susceptibility: Vulnerability or lack of
resistance.
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19. 1. Mechanical Defenses
2. Chemical Defenses
3. Cellular elements of blood
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21. I.Mechanical Defenses
Skin and Mucous Membranes
A. Skin Layers
Epidermis: Thin outer epithelial layer.
Contains Langerhans cells, dead cells, and keratin.
Dermis: Thick inner layer of connective tissue.
Infections are rare in intact skin. Exceptions…….
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22.  B. Mucous Membranes:
Lining of gastrointestinal, genitourinary, and
respiratory tracts.
 Epithelial layer secretes mucus which maintains moist surfaces.
 Although they inhibit microbial entry, they offer less protection
than skin.
 Several microorganisms are capable of penetrating mucous
membranes:
 Papilloma-virus
 Treponema pallidum
 Enteroinvasive E. coli
 Entamoeba histolytica
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23.  Lacrimal apparatus: Continual washing and
blinking prevents microbes from settling on the
eye surface.
 Saliva: Washes microbes from teeth and
mouth mucous membranes.
 Mucus: Thick secretion that traps many
microbes.
 Nose Hair: Coated with mucus, filter dust,
pollen, and microbes.
 Ciliar y Escalator: Cilia on mucous
membranes of lower respiratory tract move
upwards towards throat at 1-3 cm/hour.
 Coughing and sneezing: Expel foreign
objects.
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24. II.Chemical Defenses:
 Sebum: Oily substance produced by sebaceous
glands that forms a protective layer over skin.
Contains unsaturated fatty acids which inhibit
growth of certain pathogenic bacteria and fungi.
 pH: Low, skin pH usually between 3 and 5.
Caused by lactic acid and fatty acids.
 Perspiration: Produced by sweat glands.
Contains lysozyme and acids.
 Lysozyme: Enzyme that breaks down gram-
positive cell walls. Found in nasal secretions,
saliva, and tears.
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25.  Gastric Juice: Mixture of hydrochloric acid,
enzymes, and mucus. pH between 1.2 to 3 kills
many microbes and destroys most toxins. Many
enteric bacteria are protected by food particles.
 Helicobacter pylori neutralizes stomach acid and can
grow in the stomach, causing gastritis and ulcers.
 Transferrins: Iron-binding proteins in blood
which inhibit bacterial growth by reducing
available iron.
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26. Cell Type # Cells/mm 3 Function
Erythrocytes (RBC) 4.8-5.4 million Transport O2 and CO2
Leukocytes (WBC 5000-11000 Various
A. Granulocytes:
1. Neutrophils Phagocytosis
2. Basophils Produce histamine
3. Eosinophils Toxins against parasites
some
phagocytosis
B. Monocytes/Macrophages Phagocytosis
C. Lymphocytes Antibody production (B cells)
Cell mediated immunity (T
cells)
Platelets 300,000 Blood clotting
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27. II. Second Line of Defense
1. Phagocytosis:
 Derived from the Greek words “Eat - 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.
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28. 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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30. Stages of
Phagocytosis
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 minutes
and include:
 Lysozyme: Destroys cell wall peptidoglycan
 Lipases and Proteases
 RNAses and DNAses
After digestion, residual body with undigestable
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