Transcript ChapteInflammationr One

‫بسم هللا الرحمن الرحيم‬
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INFLAMMATION
DR:Gehan mohamed
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Inflammation

Definition: *Inflammation is the local
vascular, lymphatic and cellular reactions of
living tissue against an irritant.
*Inflammation is a protective mechanism with
the purpose of localization and removal of the
irritant.

*Inflammation is designated by adding the
suffix “itis” to the English, Latin or Greek name
of the organ affected e.g. tonsillitis,
appendicitis, gastritis ... etc.
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CAUSES OF INFLAMMATION
(1) Living Irritants: Bacteria and their toxins, viruses,
parasites and fungi.
(2) Non Living Irritants: include:
(a) Physical irritants: e.g. excess heat, excess cold
and radiations.
(b) Chemical irritants: e.g. concentrated acids, alkalis,
organic and inorganic poisons.
(c) Mechanical irritants: e.g. trauma, mechanical
friction and foreign bodies.
(3) Antigens: Cause allergic inflammation.
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TYPES OF INFLAMMATION

(1) Acute Inflammation:
 Caused by an irritant of short duration .
 The tissue response is rapid i.e. sudden
onset.
 lasts for days to weeks.
 characterized by the presence of fluid
exudates, fibrin threads and
polymorphonuclear leucocytes.
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
(2) Chronic Inflammation:
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Caused by an irritant of prolonged action.
The tissue response is slow i.e. gradual onset.
Inflammation lasts for months to years.
characterized by the presence of macrophages,
plasma cells, lymphocytes and fibrosis.
(3) Subacute Inflammation: Grades
between the acute and the chronic types.

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Acute Inflammation
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Pathogenesis of Acute
Inflammation
The acute inflammatory reaction
consists of:
I. Local tissue damage.
II. Local vascular reactions.
III. Local histiocytes reaction .
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I. LOCALTISSUE DAMAGE
Occurs at the centre of the inflamed area with the
maximum concentration of the irritant. Local
death of tissue (necrosis) will result.

This local damage of cells together with
inflammatory stimulus trigger the release and
activation of chemical substances called
chemical mediators as histamine, serotonin
and prostaglandins.
These chemical mediators play an important role in
promoting the vascular and cellular changes in
the inflamed area.
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II. LOCAL VASCULAR REACTIONS
(1)Transient vasoconstriction of the
small arterioles: Caused by the direct
effect of the irritant on the vascular wall.
Vasoconstriction is a protective mechanism
and lasts for seconds to minutes only.
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(2) Vasodilatation of the Blood Vessels:
Occurs in the arterioles, venules and
capillaries due to:
(a) Direct action of histamine on the
vascular wall.
(b) Local axon reflex.
The dilatation of the arterioles and capillaries
will increase the blood flow & is called
hyperaemia. The inflamed area becomes
red and hot.
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(3) Slowing of the Blood Stream
(Stasis): Caused by:
(a)
Increased viscosity of the blood due to
formation inflammatory fluid exudates.
This is the main cause of stasis.
(b) Histamine causes swelling of the vascular
endothelium which become sticky and
offer mechanical resistance to the blood.
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(c) Most of the capillaries in the
inflamed area open and blood
reaching the arterioles will be
distributed among large number
of capillaries, so slowing occurs.
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(4) Formation of the Inflammatory
Exudates:
The intravascular contents (plasma and
cells) escape into the interstitial tissue
spaces forming the inflammatory exudates
which consists of a fluid component and a
cellular component.
(5) Dilatation of lymphatic vessels:
to accelerate the lymph flow and drains
the fluid exudates.
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A-The Inflammatory Fluid Exudates
Mechanism of formation:
(1) Increased capillary permeability to
plasma and its proteins caused by
histamine (the main cause).
(2) Increased capillary hydrostatic pressure
due to dilatation of the arterioles and
increased blood flow. This pushes fluids
outside the capillaries.
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(3) Increased osmotic pressure of the
interstitial tissue fluid as the large protein
molecules split into smaller ones in the
process of tissue necrosis. This acts as a
suction force from the capillaries.
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Characters:
- High protein content, 4-8 gm% (the normal
interstitial tissue fluid contains 1 gm% protein).
- High fibrinogen content (turbid & clots on
standing).
- High specific gravity (above 1018).
- High cellular content (polymorphs &
macrophages)
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Functions:
(1) It dilutes toxins, chemicals and poisons,
so minimizes their effects.
(2) Brings antibodies from the blood to the
site of inflammation.
(3) Supplies nutrition for the cells and
carries away waste products.
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(4) Fibrinogen forms a fibrin network,
which acts as a mechanical barrier to
the spread of infection and as a bridge
for leucocytes to reach the irritant.
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B- The inflammatory cellular
exudates
1- Margination of leucocytes: The
polymorphs leave the axial blood stream due
to stasis and settle on the endothelial lining of
the capillaries.
2- Emigration of leucocytes: The polymorphs
push their ways between the swollen
endothelial cells through the widened pores by
means of pseudopodia to outside the vessels
by amoeboid movement.
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3- Emigration of blood monocytes: which
change in the inflamed area to macrophages
together with the tissue histiocytes.
4- Chemotaxis: Is the directed movement of
polymorphs and macrophages in the area of
inflammation towards the irritant. This is
helped by chemical products produced by
polymorphs. The inflammatory cells move
on fibrin threads.
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5- Phagocytosis: It is the ingestion and
destruction of bacteria, necrotic
debris and foreign particles by
phagocytic inflammatory cells
(polymorphs and macrophages).
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III. LOCAL REACTION OF TISSUE
HISTIOCYTES
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Late in acute inflammation the
macrophages replace the polymorphs.
Macrophages are derived from tissue
histiocytes and blood monocytes. They
phagocytose dead bacteria, necrotic debris,
pus cells and fibrin threads cleaning the
area of inflammation and preparing the
tissue for the repair process.
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CARDINAL SIGNS AND SYMPTOMS OF ACUTE
INFLAMMATION
(1) Redness: Caused by vasodilatation of
the capillaries.

(2) Hotness: Caused by arteriolar dilatation
and increased blood flow.
(3) Swelling: Caused by the vascular
dilatation and the accumulation of the
inflammatory fluid and cellular exudate.
(4) Pain: Caused by irritation of the nerve
endings by toxins and Pressure of the
inflammatory exudate on the sensory
nerves.
(5) Loss of function: due to destruction of
tissues or to avoid Pain.
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General Effects Of Acute
Inflammation
(1) Leucocytosis: Increase in the
number of polymorphonuclear
leucocytes in the blood above
l0000/cm3. Leucocytosis is caused by
the liberation of “leucocytosis
promoting factor” from the injured
tissue which stimulates the bone
marrow to produce more leucocytes.
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
(2) Fever (Pyrexia): Due to the
release of Pyrogenic substances from the
bacteria and dead leucocytes. Pyrogenic
substances disturb the function of the heat
regulating centre in the hypothalamus
causing fever. Fever disturbs the vitality of
bacteria, but is also harmful to the body as
it causes loss of fluids and electrolytes.

(3) Toxic effects: as anorexia,
headache and degeneration in
parenchymatous organs.
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FATE OF ACUTE INFLAMMATION
(1) Resolution:
Means complete restoration of the inflamed
area to normal. It occurs when tissue
damage is minimal. The products of
inflammation are rapidly removed.
Resolution is the usual course of acute
inflammation caused by mild chemical or
physical irritant, many viral infections and
lobar pneumonia.
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(2) Regression and Healing:
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The body defense overcomes the irritant.
Part of the necrotic tissue, dead cells and
fibrin are removed by the macrophages.
The rest gets liquefied.
The liquefied part together with the fluid
exudates are drained by the lymphatics
and veins. Next healing occurs by fibrosis.
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(3) Progression and Spread:

The bacteria overcome the defense mechanism
and inflammation spreads directly, by lymphatics
and by blood causing toxaemia, bacteraemia,
septicaemia or pyaemia.
(4) Chronicity:

The causative agent is partially overcomed, but
the body is unable to get rid of it completely. It
remains as a weak irritant acting on the tissue
for a long time.
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Types of acute inflammation

Suppurative
– Localized
 Abscess
Furuncle
 Carbuncle
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– Diffuse
 Cellulitis
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Non-suppurative
–
–
–
–
–
–
–
Catarrhal
Membranous
Allergic
Fibrinous
Sero-fibrinous
Hemorrhagic
Necrotizing
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I. SUPPURATIVE INFLAMMATION
(Pyogenic or Septic)
Definition: Severe acute inflammation
characterized by pus formation

Causes: Pyogenic microorganisms as
staphylococcus aureus, pneumococcus,
gonococcus and bacillus coli.
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Abscess
Definition: Localized suppurative
inflammation resulting in the
formation of an irregular cavity filled
with pus
Etiology: Caused mainly by
staphylococcus aureus which produce
coagulase enzyme that helps fibrin
formation and localize the infection.
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Sites:
Commonly the abscess occurs
in in the subcutaneous tissue
and in any organ as the lung,
brain, liver, breast.
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Characters:

the abscess shows three zones.
(a) Central zone of necrosis.
(b) Midzone containing pus.
(c) Peripheral zone of inflamed tissue called
pyogenic membrane.
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
Complications:
– Lymphangitis and lymphadenitis
– Septicemia, bacteremia and toxemia
– Septic thrombophlebitis and payemic
abscesses
– Chronicity
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Cellulitis

Definition: Acute diffuse suppurative
inflammation.
 Cause: Streptococcus haemolyticus. The
organism produces two enzymes:
(1) Fibrinolysin (streptokinase): Dissolves
fibrin.
(2) Hyaluronidase (spreading factor):
Dissolves hyaluronic acid of ground
substance helping spread of bacteria and
its toxins.
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
Sites: Loose connective tissue as
subcutaneous tissue, scrotum, upper
respiratory tract and wall of the appendix.
Characters:

(1) Failure of localization because of
absence of fibrin.
(2) Extensive necrosis.
(3) Pus is thin in consistency and may
contain many red cells i.e. sanguinous.
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Complications:
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(1) Acute lymphangitis and
lymphadenitis.
(2) Septic thrombophlebitis
causing pyaemic abscesses.
(3) Septicaemia.
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II. NON-SUPPURATIVE INFLAMMATION
1. Catarrhal Inflammation: 
Mild acute inflammation of the mucous
membranes of the respiratory and GIT
characterized by excess mucus
secretion e.g. catarrhal rhinitis
(common cold), bronchitis, ... etc.
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2. Membranous Inflammation
(Pseudomembranous)

Severe acute inflammation characterized
by the formation of a pseudomembrane on
the affected surface formed of necrotic
cells, fibrin threads, leucocytes and the
causative organism e.g. diphtheria and
bacillary dysentery.
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Pathogenesis:
 The bacteria remain on the mucosal surface
and produce powerful exotoxin which causes
patchy mucosal necrosis. The exotoxin diffuses
through the necrotic mucosa to the submucosa
causing acute inflammation. The exotoxin is
absorbed in the blood stream causing severe
toxaemia.

A yellowish white slightly elevated
pseudomembrane is formed on the surface.
The membrane is adherent and its removal
leaves a bleeding surface with the formation of
another membrane.
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3. Fibrinous Inflammation:
Characterized by an exudate rich in
fibrinogen e.g. lobar pneumonia.

4. Serofibrinous Inflammation:
It involves serous sacs as pleura,
peritoneum and pericardium.
Characterized by excess serous exudates
in the sac and deposition of fibrin on the
surface.
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5. Haemorrhagic Inflammation:
Characterized by cellular exudate rich
in the red blood cells due to vascular
damage e.g. smallpox and haemolytic
streptococcal infection.
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6. Necrotizing Inflammation:
Acute inflammation characterized by
marked tissue necrosis.
7. Allergic Inflammation:
as urticaria. It is an antigen antibody
reaction characterized by abundant fluid
exudates and eosinophils.
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CHRONIC INFLAMMATION

Chronic inflammation is characterized
by the following:
(1) The irritant is mild and has a prolonged
action.
(2) Chronic inflammation may follow acute
inflammation or starts as slowly progressing
chronic disease as in tuberculosis and
syphilis.
(3) The tissue response is gradual and
prolonged.
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
(4) The small arteries and arterioles show
thickening and narrowing called end
arteritis obliterans.
(5) The inflammatory fluid exudates is
scanty.
(6) The inflammatory cellular exudates
consists of lymphocytes, plasma cells,
macrophages and foreign-body giant cells.
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Types of Chronic inflammation:
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(1) Chronic non-specific inflammation:
Different irritants produce inflammatory
reactions of the same microscopic picture
e.g. chronic abscess and chronic tonsillitis.
(2) Chronic specific inflammation:
Each irritant or organism produces a
characteristic microscopic picture called
granuloma e.g. tuberculosis, bilharziasis
and leprosy
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Differences between acute
and
chronic inflammation
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Item
Acute inflammation
Chronic inflammation
Onset
Rapid and sudden
Slow and gradual
Duration
Short
Prolonged
Vascular
phenomena
Present
Slight or absent
Cardinal signs
Present
Slight or absent
-Polymorphs, pus cells,
macrophages
-Plasma cells,
lymphocytes,
macrophages, giant cells,
fibroblasts
-Few thick walled narrow
lumen(end arteritis
oblitrans)
Mic. Changes
Cells
Blood
vessels
-Numerous, thin walled,
dilated and filled with blood
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Granuloma
Definition: –
Chronic specific inflammation –
characterized by focal
accumulation of large number of
chronic inflammatory cells to
form tumor like mass .
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
Types
(1)Infective granuloma
1.Bacterial
as TB, leprosy & syphilis
2.Parasitic as bilharziasis &
leishmaniasis
3.Mycotic (fungus) as madura foot,
actinomycosis
4.Viral as granuloma inguinale
(2)Non-infective granuloma
 As
silicosis, asbestosis and foreignbody granuloma.
(3) Unknown cause
sarcoidosis, crohns disease
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Histopathology of granuloma
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A- Macrophages main bulk of granuloma,
made of tissue histiocytes, blood
monocytes and foreign body giant cells
B- Other inflammatory cells as
lymphocytes, plasma cells, eosinophils.
C- Granulation tissue
D- Fibrous tissue
E- Specific organism or foreign body
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Schistosomia
sis
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Schistosomiasis
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Leishmaniasis
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Leprosy
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Leprosy
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Sarcoidosis
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