.

Inflame” – to set fire Introduction

.Inflammation: defined as the vascular and cellular response of living tissue to injury
:Aim of inflammation
.The inflammatory process serves to destroy, dilute or wall-off the injurious agent *
.Repair is the process by which lost or destroyed cells are replaced by vital cells*

.'The nomenclatures of inflammatory lesion are usually indicated by the suffix 'itis Nomenclature
Thus, inflammation of the appendix is called appendicitis and that of meninges as meningitis, etc.… However,
like any rule, it has its own exceptions examples as lung is pneumonia
 Inflammation is caused by injurious agents called irritants. Irritants are of different types: CAUSES
(1) Living Irritants: Bacteria and their toxins, viruses, parasites and fungi.
(2) Non Living Irritants:
 Physical irritants: e.g. excess heat, excess cold and radiations.
 Chemical irritants: e.g. acids, alkalis, organic and inorganic poisons.
.Mechanical irritants: e.g. trauma and mechanical friction 
(3)Immunological: e.g. allergic inflammation.
Indicates the location of the lesion within an organ. Used both macro and microscopically. Distribution
FOCAL: Single abnormality or inflamed area within a tissue
MULTIFOCAL: Several foci are separated from one another by relatively normal tissue
LOCALLY EXTENSIVE: Involvement of considerable area within an organ.
DIFFUSE: Involve all the tissue or organ.

lymphocytes function primarily in the immune response (including both the humoral (B) and cell-mediated - Cells
.immunity(T) Mononuclear
.Plasma cells are committed to antibody production Ig- leukocytes
The primary function of monocytes is phagocytosis and they are termed the "second line of cellular defense.“ -
Macrophage

- Neutrophils (1) Phagocytosis ( Microphage) (2) Neutralize the toxic products of bacteria and other segmented
microorganism. nucleus
basophiles and mast cells release (heparin/histamine) in response to antigen-antibody complexes-
Eosinophils serve to degrade chemical mediators (especially histamine) by histinase -
 I- ACUTE INFLAMMATION
is an immediate and early response to an injurious agent and it is relatively of short duration defintion
.fluids and cellular exudation at the site of injury characterized
NOTE: Clinically, an acute disease is one that arises suddenly, often within a few hours, and
.progresses rather within a matter of days or a few weeks to recovery or death
1-General effects: Effects
a.Leucocytosis:Increase in the number of polymorphonuclear leucocytes.
:b. Fever (Pyrexia)
Bacteria and dead leucocytes  Pyrogenic substances (pyrexin) (fever producing)  disturb the -
function of the heat regulating center in the hypothalamus causing fever 
.Fever disturbs the vitality of bacteria, but is also harmful to the tissues of the body -
c. Degeneration and damage of parenchmatous organs as liver, kidney and, heart by absorbed
Toxins
2-Local effects:
Cardinal signs and symptoms of acute inflammation
(1) Redness: Caused by capillary vasodilatation and opening of all the collapsed capillaries.
(2) Hotness: Caused by arteriolar dilatation and increased blood flow.
(3) Swelling: Caused by the capillary vasodilatation and lead to accumulation of the inflammatory
fluid and cellular exudate.
(4) Pain: Caused by:
(a) Irritation of the nerve endings by the chemical mediators
(b) Pressure of the inflammatory exudate on the sensory nerves.
(5) Loss of function: Due to:
(c) Pain.
(d) Tissue damage.

It is characterized by the presence of fluid exudate, fibrin threads and leucocytes caused by an irritant of short duration.
The acute inflammatory reaction consists of:
I. Local tissue damage.
II. Local vascular reactions.
III. Local reaction of histocytes.
6) Cellular Exudate II. Local vascular reactions. I-LOCAL
TISSUE
DAMAGE
1) Margination of A- Transient Vasoconstriction Occurs at the
Leucocytes (1) Transient Constriction of the Blood Vessels centre of the
(Pavementing of (2) Transient rapid blood flow inflamed area as
leucocytes) : PNL (due Caused by a direct stimulating action of the irritant on the vascular wall and the causative
to stasis)  on leukotrienes . agent is at its
endothelial lining of the Vasoconstriction is a protective mechanism and lasts for seconds to minutes only. .maximum action
capillaries. B- Persistence Vasodilatation The central cells
(2) Emigration of (3) Dilatation of the Blood Vessels are killed, i.e.
Leucocytes (4) Slowing of the Blood Stream (Stasis) .necrosis
between the swollen resulted from vasoconstriction of blood vessels local damage
endothelial cells (by 3) Dilatation of the Blood Vessels: of cells 
amoeboid movement)  a-Direct action of histamine on the vascular wall. release and
outside bl. Vessel. b-The dilatation of the arterioles and capillaries with increase in the blood flow is activation of
(3) Diapedesis of Red called active hyperaemia. chemical
Cells c-The inflamed area becomes red and hot. substances
Passive pushing (4) Slowing of the Blood Stream (Stasis): Caused by: called
(Diapedesis) of Red Increased viscosity of the blood (the red blood cells become more concentrated) due to chemical
Cells by the intra- increase of permeability of the blood vessels and formation of the inflammatory fluid mediators
vascular hydrostatic exudate (protein-rich fluid moves into the extravascular tissues). 
pressure Most of the capillaries in the inflamed area open and dilate. promoting
Leukocyte Recruitment C- Inflammatory Exudate vascular
:and activation (5) Fluid Exudate and cellular
Activated leukocyte (6) Cellular Exudate changes in
products (lysosomal The inflammatory fluid exudate: the inflamed
enzymes) destroy leaves the dilated capillaries and venules due to: .area
microbes can also injure (1) Increased vascular permeability to plasma and its proteins caused by histamine and
normal host tissues kinins is the main cause.
(2) Increased capillary hydrostatic pressure due to dilatation of the arterioles and
increased blood flow.
(3) Increased osmotic pressure of the interstitial tissue fluid (decrease of intravascular
colloid osmotic pressure) . This acts as a suction force from the capillaries.
Phagocytosis is the process of engulfment and internalization by specialized cells, which includes III. LOCAL
.invading microorganisms, damaged cells, and tissue debris
REACTION OF
.These phagocytic cells include polymorphonuclear leukocytes, monocytes and tissue macrophages
:Phagocytosis involves three distinct steps - TISSUE
:Recognition HISTIOCYTES
The material to be phagocytized is coated with certain plasma proteins called opsonins. These
.opsonins promote the adhesion between the particulate material and the phagocyte’s cell membrane
.The three major opsonins are: immunoglobulin, complement and carbohydrate-binding proteins
:Engulfment
During engulfment, extension of the cytoplasm (pseudopods) flow around the object to be engulfed,
.eventually resulting in complete enclosure of the particle within the phagosome
Killing or degradation
The ultimate step in phagocytosis of bacteria is killing and degradation

Chemotaxis
The attraction of leukocytes from vascular channels towards the site of inflammation within the tissue space guided by chemical
.gradients (including virus, bacteria----- and cellular debris) is called chemotaxis
All granulocytes, monocytes and to lesser extent lymphocytes respond to chemotactic stimuli
.?How do leukocytes "see" or "smell" the chemotactic agent
This is because receptors on cell membrane of the leukocytes react with the chemo-attractants resulting in the activation of
.phospholipase C that leads to release of calcium ions and these ions trigger cell movement towards the stimulus
‫وظائف‬
, fluied exudet
(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) Supplies fibrinogen which changes to fibrin.
Fibrin has the following functions:
(a)Forms a network upon macrophages move towards the irritant.
(b) Forms a network upon which fibroblasts proliferate and start
healing.
(c) Localizes infection by surrounding the inflamed area
Formation of transudates and exudates.
A. Normal process (no fluid loss or gain)
B. Transudate is formed when fluid leaks out
because of increased hydrostatic pressure or
decreased osmotic pressure.
C. Exudate is formed in inflammation because
vascular permeability increases as a result of
increased interendothelial spaces
 TYPES OF ACUTE INFLAMMATION

Definition: Severe acute inflammation characterized by pus formation. Types of Suppurative Inflammation:
Causes: Pyogenic (pus forming) microorganisms as: (1) Localized:
staphylococcus aureus (a) Abscess, (b) Furuncle, (c) Carbuncle.
streptococcus haemolyticus, (2) Diffuse: e.g. Cellulitis, suppurative appendicitis,
pneumococcus suppurative peritonitis ... etc.
Complications of Abscess Formation

lymphangitis(inflammation of lymph vessels) .a Lymphatic)1(

.lymphadenitis (inflammation of L.Ns) .b :spread
,a: Bacteraemia (blood spread of bacteria) (2) Blood
b: Septicemia (circulation , multiplication of large number of pathogenic bacteria & their toxins in blood without spread :
.localization)
.c: Toxaemia (toxins in blood)

(3) Inadequate drainage and treatment 3

changes the abscess to a chronic one. A chronic abscess has a thick fibrous wall.
in the form of chronic ulcer, sinus and fistula (4)
ulcer : Basic description: Loss of the mucosa and deeper tissues including basement membrane the correct  Complications
.term is ulcer of healing:
.If only the mucosa is lost with intact basement membrane, the correct term is an erosion
:Microscopic morphology of an ulcer 
.The layers, from superficial to deep, are fibrin, neutrophils, granulation tissue, and fibrosis
.Location: Most commonly seen in the gastrointestinal tract and other tissues 
:Complications of an ulcer 
Pain .Hemorrhage
SINUS
blind ended tract open on surface
Fistula
Basic description: A fistula is an abnormal tunnel connecting two body cavities (hallow organ) (such as the 
.rectum and the vagina) or a body cavity to the skin (like the rectum to the outside of the body)
:Example 
Entero-cutaneous fistula .a
Biliary fistula: connecting the bile ducts to the skin surface, often caused by gallbladder surgery .b
Rectovaginal fistula: between the rectum and vagina .c
Definition: Abscess
A localized suppurative inflammation resulting in the formation of an irregular cavity containing pus.
Cause: Commonly Staphylococcus aureus.
Site: Commonly the abscess occurs in the subcutaneous tissue, but occur in any organ as the lung, brain, liver ... etc.
Composition of Pus:
(1) Bacteria living and dead and their toxins.
(2) Liquefied necrotic tissue.
(3) Inflammatory cellular exudate in the form of polymorph- leucocytes, many pus cells, macrophages and red cells.
(4) Inflammatory fluid exudate.
Pathogenesis of Abscess Formation
1.Pyogenic microorganisms cause tissue necrosis by its toxins and exert strong chemotaxis on polymorph-nuclear
leucocytes.
2.Many leucocytes (neutrophil) are killed during their struggle bacteria and are called pus cells.
3.The dead leucocytes (pus cells) release proteolytic enzymes which cause rapid liquefaction of the necrotic tissue.
.The resulting fluid material mix with the fluid and cellular exudate forming the pus
Microscopically: (zone formation)
Early: - central necrotic tissue and
.peripheral area of acute inflammation surround it -
.Late: - central necrotic tissue
.pus cavity surround it -
.area of acute inflammation [ pyogenic membrane] surround it with excess neutrophils -
N/E : cardinal signs of acute inflammation
 SUPPURATIVE / PURULENT - ABSCESS
.Fate of abscess : pus in body must be evacuated
: Pus can be evacuated either
Surgical method : healing. 2. Spontaneously .1
.Small abscess related to a hair follicle or sebaceous gland caused by staphylococcus aureus Furuncle
Common sites are face and back of the neck in males and axilla in females. (Boil)
Multiple furuncles are called furunculosis.
Definition: A type of localized suppuration forming multiple communi­cating suppurative foci in the skin and Carbuncle
.subcutaneous fat discharging pus through several openings
.Cause: Staphylococcus aureus. Diabetes mellitus is a common predisposing factor
Sites: Areas where the skin and subcutaneous tissue are thick and tough as the back of the neck and buttocks.
 B-DIFFUSE SUPPURATIVE INFLAMMATION
Cellulitis (Phlegmonous Inflammation))
 Definition: Acute diffuse suppurative inflammation.
 Cause: Streptococcus haemolyticus.
 The organism produces two enzymes:
.Fibrinolysin (streptokinase): Dissolves fibrin )1(
(2) Hyaluronidase (spreading factor): Dissolves hyaluronic acid of ground :Complications
substance helping spread of bacteria and its toxins.
 Sites: Loose connective tissue as subcutaneous tissue .Acute lymphangitis and lymphadenitis )1(

.Septicemia )2(
Pathology of Cellulitis
The basic pathological changes are similar to those of abscess with the
:following differences

Failure of localization because of absence of fibrin (No pyogenic )1(

.membrane)

The necrosis is extensive )2(

Pus formation is slow. Pus is thin in consistency and may contain many )3(
.red cells i.e. sanguineous
 by excess serous exudate - thin fluid that is derived from either the blood serum or secretion of mesothelial cells Serous -1
lining serous cavities.
e.g. burns and herpes simplex.
Serous inflammation usually observed in the serous membranes
e.g. pleura, pericardium, synovial membrane and peritoneum.
 exudate rich in fibrinogen which converted to fibrin. -2
 The fibrin mixed with inflammatory cells mainly neutrophils, macrophages and plasma cells. Fibrinous
 in mucous and serous membrane.
excess fluid exudate rich in fibrin Sero- -3
 Gross Picture: Fibrinous
 (a) Early the serous surfaces show many hyperaemic vessels.
 (b) Next the visceral and parietal layers become thickened, opaque, grayish yellow
 collects in the serous sac.
 Microscopic Picture
 a) The fibrinogen changes to fibrin forming a network on visceral and parietal layers entangling acute
inflammatory (polymorphs, pus cells, macrophages and RBCs).
 (b) The serosa shows hyperaemia, inflammatory oedema, acute inflammatory cells & fibrin.
excess mucus secretion e.g. catarrhal rhinitis, bronchitis .4
Gross Picture: Catarrhal
(a) Early the mucous membrane appears red, hot, swollen and dry. Dryness is due to temporary cessation of mucus
secretion.
(b) Then excess watery mucoid discharge appears, composed of inflammatory fluid exudate, mucus, small number
of polymorphonuclear leucocytes and shaded epithelial cells.
When the polymorphs increase the discharge becomes thick and yellowish.
Microscopic Picture
(a) Mucosal cells appear swollen and rounded due to mucus accumulation and may rupture or desquamate.
(b) The submucosa shows hyperaemia, inflammatory oedema and mild PNL leucocytic infiltration.
formation of a pseudomembrane e.g. diphtheria )Pseudomembranous or Diphtheritic( -5
 Pathogenesis: Membrano
 The bacteria produce powerful exotoxin which causes patchy mucosal necrosis. us
 The exotoxin is absorbed in the blood stream causing severe toxaemia
 Gross Picture:
Early the mucosa is congested and shows small grayish yellow patches of necrosis.
Next a yellowish white patches slightly elevated, pseudomembrane is formed on the surface.
The membrane is adherent and its removal leaves a bleeding surface

‫ رحاب الخوتاني‬: ‫اعداد الطالبة‬

 cellular exudate rich in red blood cells due to vascular damage -6
.e.g. smallpox and anthrax Haemorrh
Hemorrhagic pancreatitis agic

.marked tissue necrosis e.g. Viral hepatitis, Typhoid fever -7

Necrotizin
g

cellular reaction mainly eosinophils and mast cells. Allergic-8

The main cause of allergy is progressive reaction of human body against certain foreign protein e.g. bronchial
asthma, drug, food, pollution.

COURSE OF ACUTE INFLAMMATION

Resolution :  normal tissues
:Regression and Healing
.The body defense overcomes the irritant
Necrotic tissue removed by macrophages
Liquified parts drained by lymphatics
:Progression and Spread )3
.The bacteria overcome the defense mechanism
.Inflammation spreads directly, by lymphatics &blood causing fatal septicaemia
:Chronicity )4
.The body is unable to get rid the bacteria completely
It remains as a weak irritant acting on the tissue for a long time  chronic inflammation