Short notes about :

INFLAMMATIO
N

INFLAMATION

Is the local vascular

,lymphatic,cellular reactions of
living tissue against na irritant
(injurios agent) .

CAUSES OF INFLAMATION

Antigens:cause allergic inflamation

Living irritants:bacteria and their
toxins,viruses,parasites and fungi.
Non-living irritants :
a-physical irritants
b-chemical irritants
c-mechanical irritants

TYPES OF INFLAMATION

Acute inflamation
-caused by na irritant of short duration of
action
- rapid onset
-lasts for days to weeks
-characterized by presence of fluid exudate
fibrin threads and polymorphonuclear
leucocytes

TYPES OF INFLAMATION

Chronic inflamation
-caused by na irritant of prolonged action
- slow rapid of onset
- lasts for monthes to years
-Characterized by the presence of
macrophages ,plasma cells,lymphocytes nand
fibrosis .

TYPES OF INFLAMMATION

Subacute inflammation
grades between the acute and choronic
inflammation .

ACUTE INFLAMMATION
Consists of :
I.Local tissue damage
II.Local vascular reactions
III.Local reactions of tissue histiocytes.

LOCAL TISSUE DAMAGE

Occures at the centre of the inflammed area

The irritant is at its maximum action
The central cells are killed
The surronding cells are less severly injured
chemical mediators:
(histamin,serotonin,prostaglandins and
others) play na important role in promoting
the vascular and cellular changes in the
inflammed area .

LOCAL VASCULAR REACTIONS

Transient constriction of the blood vessels
-caused by a direct stimulating action of the
irritant on the vascular wall
-lasts for seconds to minuts
Dilatation of the blood vessels
-occurs in the arterioles,capillaries,and
venules
Slowing of the blood stream
Formation of the inflammatory exudate

THE INFLAMMATORY CELLULAR

EXUDATE

The inflammatory fluid exudate leaves the dilated

capillaries and venules due to:
- increased vascular permeability to plasma and its
proteins caused by histamine and kinins
- increased capillary hydrostatic pressure due to
dilatation of the arterioles and increased blood flow
-increased osmotic pressure of the interstitial tissue fluid
.
-the ground substance becomes more fluid in structure
due to depolymerization of its mucopolysaccharides

THE INFLAMMATORY CELLULAR EXUDATE

Margination of leucocytes
-the polymorphonuclear leucocytes leave the
axial blood stream due to stasis
Emigration of leucocytes
-thpolymorphonuclear leucocytes push their
way between the swollen endothelial cells
Emigration of monocytes
-the monocytes and histocytes in the
inflammed area change to macrophages

THE INFLAMMATORY CELLULAR

EXUDATE

Diapedesis of red cells

-is the mechanical pushing of the red cells which
have a small diameter by intravascular pressure
Chemotaxis
-is the directed movment of the
polymorphonuclear leucocytes and macrophages
in the area of inflammation,towards the irritant
Phagocytosis
-is the ingestion and destruction of the bacteria
necrotic debris and foreign particles by
phagocytic inflammatory cells

LOCAL REACTION OF TISSUE

HISTIOCYTES

The macrophages replace tha

polymorphonuclear leucocytes in the late
acute inflammation
Macrophages derived from tissue histiocytes
and blood monocytes
The phagocyose the dead bacteria ,necrotic
debris,pus cells and fibrin threads cleaning
the area of inflammation

CHEMICAL MEDIATORS OF ACUTE

INFLAMMATION

Are chemical factors derived from plasma

and cells
(neutrophilis,monocytes,macrophages ,mast
cells ,endothelium,smooth
muscles,fibroblasts and platelets)

They are acting by binding to specific

receptors on the target cells

CHEMICAL MEDIATORS OF ACUTE

INFLAMMATION

Cellular factores
1-vaso active amines
-as histamin and serotonin released from
mast cells
2-arachidonic acid
-prostaglandins
-leukotriens are produced by neutrophilis
3-lysosomal components
- released fron neutrophils macrophages and
platelets
4- cytokines
-lymphokines from activated lymphocytes and monokines
from activated mono nuclear phagocytes

CHEMICAL MEDIATORS OF ACUTE

INFLAMMATION

Plasma factors
1-kinin system
2-complement system
-complement components specially C3a
and C5a
3-coagulation system
- changes fibrinogen to fibrin
4-fibrinolytic system
-dissolvis fibrin

THE MAIN ACTIONS OF THE

CHEMICAL MEDIATORS

Vascular dilatation
-caused by histamin prostaglandins C3a
and C5a
Increased vascular permeability
-caused by histamin ,kinin ,leukotrienes
and prostaglandins
chemotaxis
-caused by leukotrienes and lysosomal
components.

CARDINAL SIGNS AND SYMPTOMS

OF ACUTE INFLAMMATION

Redness
Hotness
Swelling
Pain
Loss of function

TYPES OF ACUTE
INFLAMMATION

Suppurative inflammation
Non-supurative inflammation
1-catarrhal inflammation
2-membranous inflammation
3-sero-fibrinous inflammation
4-fibrinous inflammation
5-serous inflammation
6-haemorrhagic inflammation
7-necrotizing inflammation
8-allergic inflammation

SUPPURATIVE INFLAMMATION

Sever acute inflammation characterized by pus

formation
Pus :

Pathogenesis of pus formation:

-pyogenic microorganisms cause marked tissue necrosis by its
toxins and exert strong chemotaxis
-many leucocytes are killed during their struggle witht the
bacteria
-the dead leucocytes release proteolytic enzymes which cause
rapid liquefction of the nercotic tissue and the fibrin threads.
- the resulting fluid material mix with the other inflammatory
process forming the pus

TYPES OF SUPPURATIVE
INFLAMMATION
Localized
-abscess
-furuncle
-carbuncle
Diffuse
-cellulitis
- suppurative appendcitis
-suppurative peritonitis

ABSCESS

a localizes suppurative inflammation

resulting in the formation of an irregular
cavity containing pus

Commonly abscess occurs in the

subcutaneous tissue,lungs ,brain,liver..etc

FURUNCLE

Small abscess related to a hair follicle or

sebaceouos gland caused by staphylococcus
aureus

Common sites are face and back of the neck

in male and axilla in females

CARBUNCLE

A type of localized suppurative forming

multiple communicating suppurative foci in
the skin and subcutaneous fat discharging
pus through sevral openings

The most common sites are the area where

the skin and subcutaneous tissue are thick
and tough as the back of the neck ,scalp and
buttocks

DIFFUSE

Cellulitis :
-acute diffuse suppurative inflamation
- commonly found in loose connective tissue
as subcutanous tissue ,facial planes,areolar
tissue of the orbit ,pelvis ,scrotum and wall
of the appendix.

NON-SUPPURATIVE
INFLAMMATION
Catarrhal inflammation
-mild acute inflamation of the mucouse
membranes charactrized by excess mucus
secration
Gross picture:
- early the mucous membrane appears red,hot
,swollen and dry
- the excess watery mucoid discharge appears
composed of inflammatory fluid exudate ,mucus
small number of polymorphonuclear leucocyts
and sheded epethelial cells

NON-SUPPURATIVE
INFLAMMATION
Microscopic picture
-mucosal cells appear swollen and rounded
due to mucus accumulation

- the submucosa shows hyperaemia

,inflammatory odema and mild
polymorphonuclear leucocytic infiltraion.

NON-SUPPURATIVE
INFLAMMATION

Membranous inflamation
Sever acute inflammation charcterized by
formation of pseudomembrane on the
affected surface
Gross picture:
-early the mucosa is congested and shows
small greyish yellow patches of necrosis
-next a yelloiwsh white slightly elevated
pseudomembrane is formed on the surface.

NON-SUPPURATIVE
INFLAMMATION
Microscopic picture:
- the pseudomembrane is formed of necrotic
mucosal cells ,bacteria,and acute
inflammatory cells held together by fibrin
network
- the submucosa shows hyperaemia
inflammatory odema ,fibrin network and
acute inflammatory cells .

NON-SUPPURATIVE
INFLAMMATION

Sero-fibrinous inflammation
- acute inflammation charactrized by the
formation of excess fluid exudate rich in
fibrinogen e.g inflammation in serous sacs

gross picture:
-early the serous surfaces show many hyperaemic
vessels
-next the visceral and parietal layers become
thickened ,opaque ,greyish and reticulated due
to fibrin deposition
- na inflammatory serous fluid collects in the
serous sac

NON-SUPPURATIVE
INFLAMMATION
Microscopic picture :
-serosal cells lining the visceral and parietal
layers swell due to degeneration and
desquamate leaving bare surface.
-na inflammatory fluid exudate rich in
fibrinogen pours from the bare surface
- the subserosa shows hyperaemia
,inflammatory odema ,fibrin,network and
acute inflammatory cells .

NON-SUPPURATIVE
INFLAMMATION

Fibrinous inflammation

-acute inflammation charctrized by na

exudate rich in fibrinogen e.g labor
pneumonia
-

NON-SUPPURATIVE
INFLAMMATION

Serous inflammation
- acute inflammation charcterized by excess
serous exudate e.g mild burns and herpes
simplex which show epidermal vesicles full of
serous fluid containing few inflammatory
cells

NON-SUPPURATIVE
INFLAMMATION

Haemorrhagic inflammation
-acute inflammationcharcterized by cellular
exudate rich in the red blood cells due to
vascular damage e.g smallpox and
haemolytic streptococcal infection

NON-SUPPURATIVE
INFLAMMATION

Necrotizing inflammation

-acute inflammation charctrized by marked

tissue necrosis e.g cancrum oris

CHRONIC INFLAMMATION

The irritant is mild

May follow acute inflammation
The tissue response is gradual and prolonged
Tissue necrosis in progressive and gradually
replaced by fibrous tissue
Vascular dilatation and congestion are mild
The inflammatory fluid exudate is scanty

CHRONIC INFLAMMATION

The exudate shows the following types of the

inflammatory cells :
- lymphocytes
- plasma cells
- macrophages

TYPES OF CHRONIC
INFLAMMATION

Chronic non-specific inflammation

- different irritants produce inflammatory
reactions of the same microscopic picture
- this type may follow the acute inflammation

Chronic specific inflammation

-each irritant produces inflammationof a
charcteristic microscopic picture

GRANULOMAS
Is a type of chronic specific inflammation
characterized by focal accumulation of larg
number of macrophages together with
lymphocytes,plasma cells,gaint cells .
Types :
-infective granuloma
-non infective granuloma
-granuloma of unknown cause