This document discusses inflammation. It defines inflammation and its causes, which include living and non-living irritants. It describes the two main types of inflammation - acute and chronic. Acute inflammation is rapid in onset while chronic inflammation is gradual. The five signs of acute inflammation are also outlined. The pathogenesis of acute inflammation involves local tissue damage triggering chemical mediators that cause vascular changes and leukocyte response. This leads to cardinal signs like redness, swelling, heat and pain. The document also discusses different types of acute inflammation such as suppurative and non-suppurative.

1. ‫الرحي‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬‫م‬
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2. INFLAMMATION
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3. Inflammation
Definition: *Inflammation is the local 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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4. 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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5. 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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6. (2) Chronic Inflammation:
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.

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7. Acute Inflammation
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8. The five cardinal signs of acute
inflammation
Redness (rubor) which is due to dilation of small
blood vessels within damaged tissue as it occurs in
cellulitis.
Heat (calor) which results from increased blood
flow (hyperemia) due to regional vascular dilation
Swelling (tumor) which is due to accumulation of
fluid in the extravascular space which, in turn, is due
to increased vascular permeability.
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9. Pain (dolor), which partly results from the
stretching & destruction of tissues due to
inflammatory edema and in part from pus under
pressure in as abscess cavity.
Some chemicals of acute inflammation, including
bradykinins, prostaglandins and serotonin are also
known to induce pain.
Loss of function: The inflammed area is inhibited
by pain while severe swelling may also physically
immobilize the tissue.
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10. Pathogenesis of Acute inflammation
mediators play an important role in
promoting the vascular and cellular
changes in the inflamed area.
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11. 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 inflamthe
vascular and cellular changes in the inflamed
area. matory 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
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12. Pathogenesis of Acute
Inflammation
The acute inflammatory reaction consists of:
1) An early vascular and
2) A late cellular responses.
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13. I. LOCAL VASCULAR REACTIONS
(1)Transient vasoconstriction of the small arterioles:
Caused by the direct effect of the irritant on the vascular
wall. Chemical & neurogenic stemuli
Vasoconstriction is a protective mechanism and lasts for
seconds to minutes only.
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14. (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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15. (3) Slowing of the Blood Stream
(Stasis): Caused by:
slowing of blood flow & stasis due to increased
vascular permeability that is most remarkably
seen in the post-capillary venules.
Increased viscosity of the blood due to
formation inflammatory fluid exudates. This is
the main cause of stasis.
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16. (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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17. Mechanism of formation of the exudate :
1-ncreased 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.
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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18. Characters:-
1-High protein content, 4-8 gm% (the
normal interstitial tissue fluid contains 1
gm%protein).
2-High fibrinogen content (turbid &
clots on standing). -High specific
gravity (above 1018).
3-High cellular content (polymorphs &
macrophages)
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19. 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.
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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20. Characteristically, the acute inflammatory
response involves production of exudates.
An exudate is an edema fluid with high
protein concentration, which frequently
contains inflammatory cells.
A transudate is simply a non-inflammatory
edema caused by cardiac, renal,
undernutritional, & other disorders.
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22. 2) Cellular response
The cellular response has the following stages:
1) Margination, rolling, pavementing, & adhesion
of leukocytes
2) Transmigration of leukocytes
3) Chemotaxis
4). Phagocytosis
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23. A, Normal axial flow of
blood with central column
of cells and peripheral
zone of cell-free plasma.
B, Margination and
pavementing of
neutrophils with narrow
plasmatic zone.
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24. C, Adhesion of
neutrophils to
endothelial cells with
pseudopods in the
intercellular junctions.
D, Emigration of
neutrophils and
diapedesis with
damaged basement
membrane.
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25. 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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26. 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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 Suppurative
Localized
Abscess
Furuncle
Carbuncle
Diffuse
Cellulitis
 Non-suppurative
 Catarrhal
 Membranous
 Allergic
 Fibrinous
 Sero-fibrinous
 Hemorrhagic
 Necrotizing
Types of acute inflammation

32. 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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33. 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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34. Sites:
Commonly the abscess occurs in in
the subcutaneous tissue and in
any organ as the lung, brain, liver,
breast.
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35. 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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36.  Complications:
 Lymphangitis and lymphadenitis
 Septicemia, bacteremia and toxemia
bactremia…carriage of small numbers of bacteria
without growth in the blood stream.
SepticemiaIs the circulation of large number of
virulent micro-organism with multiplication and toxin
production in the circulation. This commonly leads to
septic shock.
Toxemia…means circulation of bacterial toxins in
blood with clinical and pathological manifestations
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37.  Septic thrombophlebitis and payemic
abscesses
 Chronicity
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44. 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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45.  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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46. Complications:
 (1) Acute lymphangitis and lymphadenitis.
 (2) Septic thrombophlebitis causing
pyaemic abscesses.
 (3) Septicaemia.
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50. 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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51. 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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52. 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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53. 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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54. 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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57. 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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58. 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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59.  (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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61. Types of Chronic inflammation:
 (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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62. Differences between acute
and
chronic inflammation
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63. Chronic inflammationAcute inflammationItem
Slow and gradualRapid and suddenOnset
ProlongedShortDuration
Slight or absentPresentVascular
phenomena
Slight or absentPresentCardinal signs
-Plasma cells,
lymphocytes,
macrophages, giant cells,
fibroblasts
-Few thick walled narrow
lumen(end arteritis
oblitrans)
-Polymorphs, pus cells,
macrophages
-Numerous, thin walled,
dilated and filled with blood
Mic. Changes
Cells
Blood vessels
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64. 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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65. 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 foreign-body
granuloma.
(3) Unknown cause
sarcoidosis, crohns disease
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66. Histopathology of granuloma
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

68. 68
Schistosomiasis

69. Leishmaniasis 69

70. Leprosy 70

71. Leprosy
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72. 72Sarcoidosis

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