Inflammation

Presented
By
Ahmed El-Rashedy
Professor & Previous Head
of Pathology Department
Al-Azhar University

Prof. Dr. Ahmed Elrashedy

Inflammation
Def.: It is a series of vital reaction of a living tissue in
response to an irritant.
Types of irritants: Irritant is a stimulus causing either
reversible or irreversible cell injury. Irritants include:
1. Physical agents: Heat, Coldness, Trauma, Severe
pressure.
2. Chemical agents: Acids, Alkali, Corrosives.
3. Irradiations: whether ionizing or non-ionizing.
4. Allergens: whether injectable (aspirin, penicillin) ,
Ingestible drugs ( sulphonamide) or foods as egg,
chocolate, fish, meat or inhaled as dust or perfumes.
5. Biological agents: Fungi, Bacteria, Viruses,
Parasites, etc.

Prof. Dr. Ahmed Elrashedy

Classification: Two types:

1. I) Acute inflammation: subdivided into two:
1.Suppurative ( Septic) : subgrouped into two:
A) Localized:
a) Abscess.
b) Boil ( Furuncle).
c) Carbuncle.
B) Diffuse ( Cellulitis = Phlegmonous inflammation).
2. Non-suppurative: This includes:
A) Allergic.
E) Serofibrinous.
B) Membranous.
F) Fibrinous.
C) Catarrhal.
G) Gangrenous.
D) Serous.
H) Hemorrhagic.

Prof. Dr. Ahmed Elrashedy

II) Chronic inflammation: subdivided into two:

1. Specific ( GRANULOMAS): Two types:
A) Infected granulomas include:
a) Bacterial:
1. T.B.
2. Syphilis.
3. Leprosy.
4. Rhinoscleroma.
b) Parasitic:
1. Bilharziasis.
2. Toxoplasmosis.
c) Fungal:
1. Actinomycosis.
2. Histoplasmosis.
B) :Non infective granulomas include:
1. F.B. granulomas ( Foreign suture granuloma &
Pneumoconiosis e.g. silicosis, asbestosis, byssinosis).
2. Sarcoidosis.
3. Immunological granulomas (Ashoff myocarditis,
Sperm head granuloma).
2. Non-specific: complicates acute inflammation ; e.g. chronic
non-specific abscess.

Prof. Dr. Ahmed Elrashedy

Acute

Chronic

1. Onset
2. Irritant

Sudden
Severe.

Gradual
Mild.

3. Duration

Short ( days- weeks)

Longer (months-years)

4. Course

Rapidly progressive

Slowly progressive

5. Exudate:
A) Fluid part.
B) Cellular part

Excess
Moderate

Little
Excess

Polymorphs (Neutrophils).
Pus cells ( Dead polymorphs).
RBCs.
Macrophages.
Eosinophils.

Plasma cells.
Lymphocytes.
Macrophages(Histiocytes).
Giant cells.
Fibroblasts.
Eosinophils.
From tissue histiocytes.

6. Types of cells

7.
Origin
of From blood monocytes.
macrophages
8. Arrangement
Diffuse.
9. Vascular changes Mild.

Perivascular or diffuse.
Marked.

Prof. Dr. Ahmed Elrashedy

Acute

Chronic

10. Blood vessels

Congested, dilated & thinwalled

Little congested , narrow

lumen & thick - walled
( End-arteritis obliterans).

11. Repair

Follow.

Associate.

12.Granulation tissue

Absent

Present

13.Fibrosis

Absent

Marked.

14.Toxemia

Severe.

Mild.

15.CardinalSigns

Redness hotness
Absent except swelling.
pain swelling loss of
function.
present.
usually absent.
Total
leucocytic count is normal
or decrease

16.General changes as
fever and leucocytosis

17.Types

Suppurative or non sup. Specific or non - specific.

Prof. Dr. Ahmed Elrashedy

Effects of Acute Inflammation

I) Local ( Cardinal signs & symptoms):
1.Redness:due to capillary vasodilatation.
2.Hotness: due to arteriolar vasodilatation.
3.Swelling:due to inflammatory exudate formed as a result of capillary
vasodilatation.
4.Pain & tenderness: due to
A) Increased tissue tension by the inflammatory exudate.
B) Irritation of the nerve endings by waste products of inflammation.
5. Loss of function: due to pain & tissue damage.
II) General:
1. Fever: due to absorption of pyrexin produced by organisms or dead
polymorphs.
2.Leucocytosis: due to b.m. stimulation by leucocytosis promoting
factor.
3. Degeneration and damage of the parenchymatous organs (liver,
kidney & heart) by the absorbed toxins.

Prof. Dr. Ahmed Elrashedy

Chemical Mediators
Def.: They are chemical substances released in response to an
inflammatory process mediating it.
Origin:
1. Plasma.
2. Inflammatory cells.
3. Damaged tissue.
Classification: They are classified into:
1. Group I: Vasoactive amines as histamine & serotonin.
2. Group II: plasma proteases which are subdivided into:
A) Kinin system: as Bradykinin & Kallikerin.
B) Complement system: particularly C3a, C5a, C5b, C9.
C) Coagulation-fibrinolytic system: as fibrinopeptides & fibrin
degradation products.
3.Group III: Arachidonic acid derivatives as prostaglandins &
leukotrienes.
4.Group IV: Lysosomal constituents as acid proteases (acting on
intracellular proteins) & neutral proteases (acting on extracellular
proteins).

Prof. Dr. Ahmed Elrashedy

Action

Type of chemical mediators

1. Vasoconstriction

Leukotrienes.

2. Vasodilatation

Prostaglandins.

3. Increased Capillary
permeability

Leukotrienes.
Vasoactive amines (Histamine & Serotonin).
Bradykinin.
Complements ( C3a & C5a ).
Platelet activating factor (PAF).

4. Pain

Prostaglandins.
Bradykinin.

5. Fever

Prostaglandins.
Interleukin -1(IL-1) & Tumor necrosis factor (TNF).

6. Chemotaxis

Leukotrienes.
C5a.
Bacterial Products.

7. Tissue damage

O2 derived free radicals.

Lysosomal constituents (Proteases).

Prof. Dr. Ahmed Elrashedy

Phenomenon of Acute Inflammation

I. Local tissue damage (Cell injury).
II. Local vascular phenomenon.
III. Repair.
IV. Local vascular phenomenon:
1. Initial Temporary vasoconstriction.
2. Vasodilatation of the arterioles causing :
A)Hyperperfusion (increased blood flow) to the affected
area.
B) Increased hydrostatic vascular pressure.
3.Vasodilatation of the capillaries &venules causing:
A) Slowing or stasis of the blood flow.
B) Increased capillary permeability leading to escape
of fluid exudate (plasma proteins & fibrin) into the
extracellular component with resultant more viscid blood.

Prof. Dr. Ahmed Elrashedy

Local Vascular Phenomenon

4. Formation of the cellular exudate:
A) Pavementation or Margination: Leukocytes leaves the axial zone of
the blood stream and adhere to the swollen endothelium as a result of the
action of chemical mediators such as C5a, IL-1, TNF, PAF, plasma
Proteases.
B) Emigration: Escape of the leukocytes through amoeboid movement by
formation of pseudopodes into extracellular compartment without destruction
of the vessel wall.
C) Diapedesis: Passive escape of red cells through temporary hole in the
vascular wall (following emigration) into extracellular compartment because
the diameter of red cells is smaller than that of leukocytes.
5. Formation of the inflammatory exudate:
Finally, the fluid & cellular exudates are formed in the extracellular
compartment of the inflamed area. The fluid exudate washes the inflamed
area and return back into the general circulation through lymphatics & veins
while the cellular exudate is responsible for the immune response against
the irritant.

Prof. Dr. Ahmed Elrashedy

Inflammatory Exudate: Two components

1. Fluid exudate.

Fluid exudate
2. Cellular exudate.
1. Composition:

High protein (4-8 gm %).

High
specific
gravity
>1018.
High fibrinogen.

Cellular exudate
Acute inflammatory cells:
Polymorphs or neutrophils or
polymorphonuclear
leukocytes
(PNLs) .
Pus cells (dead PNLs).
Macrophages.
Eosinophils & Mast cells.
RBCs.
Chronic inflammatory cells:
Lymphocytes.
Plasma cells.
Macrophages or Histiocytes.
Giant cells.
Eosinophils.
RBCs.
Fibroblasts.

Prof. Dr. Ahmed Elrashedy

2. Function:

Fluid exudate

Cellular exudate

Dilution of toxins.
Provides
antibodies
(antitoxins & precipitins).
Fibrin acts by:
1.Blocking the meshes of
the tissue &thus localizing
the infection.
2. Acts as a scaffold or
railway upon which PNLs
traverse.
3. Helps the repair which
starts early at the site of
fibrin.

1.PNLs:
Active phagocytosis that is the engulfing of
irritant & digesting it through release of their
mediators (lysosomal or lytic enzymes).
2. Macrophages( Scavenger cells):
They are derived from blood monocytes thus
they engulf microorganisms and necrotic
debris converting them into soluble
substances through their own lysosomal
enzymes as well as wash them out to
prepare the inflamed area for healing.
3.Eosinophils:
They are increased (eosinophilia) in :
a)Allergic conditions: as Urticaria &
Bronchial asthma.
b) Parasitic diseases: as Bilharziasis,
Amoebiasis , Leishmaniasis..etc.
They produce IgE.
4. Mast cells: They release vasoactive
amines that act in the inflammatory process.

Prof. Dr. Ahmed Elrashedy

Fluid exudate
2. Function:

Cellular exudate
5. Lymphocytes:
They function in both humoral (B-cells) & in
cell-mediated response( T- cells that produce
lymphokines group of chemical mediators).
6. Plasma cells:
They arise from B-lymphocytes & function in
humoral immunity through producing
immunoglobulins (antibodies).
7. Giant cells:
They function in phagocytosis of F.B. ,
bacteria or tumor cells.
8. Fibroblasts:
Active cells synthesize the collagen fibers,
growth factors and proteoglycans of ground
substance & basement membranes.

Prof. Dr. Ahmed Elrashedy

Differences Between Exudate and

Transudate
Exudate

Transudate

High ( > 3 gm % )

Low ( < 3 gm % )

High

Low

3. Cellular content

Hypercellular
(rich in cells)

Hypocellular
(Poor in cells)

4. Specific gravity

> 1018

< 1018

5.Coagulation on standing

Present

Absent

6. Origin

Plasma

Interstitial fluid
or serous fluid

Inflammation

Oedema & CVC

1. Protein content
2. Fibrinogen content

7. Example

Prof. Dr. Ahmed Elrashedy

Acute Inflammation
Suppurative ( Pyogenic or Septic)
Localized
1. Abscess.
2. Boil (Furuncle = small abscess).
3. Carbuncle ( Multilocular abscess).
I)Abscess
Def.:
Localized suppurative inflammation caused mainly
by staphylococci.
Pathogenesis:
Staphylococci produce coagulase enzyme that
converts fibrinogen into fibrin , thus, localizes the
infection.

Prof. Dr. Ahmed Elrashedy

I) Abscess

Pathology:
A) Early:
The abscess is formed of two layers:
1. Central core of necrotic tissue.
2. Outer pyogenic layer.
B) Late:
1. Central core of necrotic tissue.
2. Intermediate pus ( by liquefaction of the necrotic
tissue).
3. Outer pyogenic layer.
N.B. Pus is formed of :
1.Liquefied necrotic tissue.
2.Living & dead bacteria.
3.Living & dead polymorphs.
4.Fluid exudate.
5.Fibrin threads.
6.Few RBCs.

Prof. Dr. Ahmed Elrashedy

I) Abscess
Fate :
Due to the increased osmotic pressure inside the abscess, fluid is dragged
from the surroundings with increased tension within the abscess causing
severe throbbing pain followed by spontaneous rupture & drainage.
Complications:
A) Local:
1. Sinus:
A tract with one opening joining the abscess cavity with skin surface.
2. Fistula:
A tract with two openings joining two hollow organs or a hollow organ with
skin surface.
3. Ulcer :
Persistent loss of the epithelial continuity.
4. Chronicity:
A conversion of acute into chronic abscess (Table discussed later).
5. Local spread:
Dissemination into the surrounding tissues e.g. pyogenic liver abscess
spreads into the lung.

Prof. Dr. Ahmed Elrashedy

I) Abscess
B) Systemic:
1. Toxemia: Presence of bacterial toxins (whether endotoxins or exotoxins)
circulating in the blood stream.
2. Bacteremia: Temporary presence of only low virulent bacteria circulating in
the blood stream usually without any symptoms (asymptomatic).
3. Septicemia: Presence of highly virulent bacteria & their toxins circulating in
the blood stream.
4. Pyemia: Presence of bacterial clumps or septic emboli circulating in the blood
stream to reach organ(s) causing multiple abscesses.
It is two types:
a)Portal pyemia: Septic emboli carried to the liver by portal circulation.
b)Systemic pyemia: Septic emboli carried to different organs including the liver
by general circulation.
5. Systemic spread:
a)Through lymphatics (Lymphangitis) into the draining lymph nodes
(lymphadenitis).
b)Through systemic or pulmonary circulation giving pyogenic single abscess in
different organ or lung respectively.

Prof. Dr. Ahmed Elrashedy

Differences Between Acute & Chronic

Abscess
Acute abscess

Chronic abscess

Irregular & shreddy

Regular & smooth

2. Content

Profuse thin pus

Little thick pus

3. Cell type

Acute inflammatory cells

Chronic inflammatory cells

By incision

By excision

Absent

May occur

1. Wall

4. Treatment

5. Calcification

Prof. Dr. Ahmed Elrashedy

II)Boil (Furuncle)
Def.: It is a small abscess related to hair follicle or to a sebaceous gland.
Multiple small abscesses related to several hair follicles cause a condition
known as Furunculosis.
III) Carbuncle
Def.: It is multilocular abscess with multiple sinuses discharging pus.
Site: It occurs commonly in the nape (back of the neck) of a diabetic
patient.
Acute Inflammation
Suppurative ( Pyogenic or Septic)
Diffuse ( = Cellulitis)
Def.: Cellulitis is a diffuse acute suppurative inflammation caused by
streptococci.
Pathogenesis: Streptococci release lytic enzymes (hyaluronidase &
fibrinolysin) that produce lysis of the tissue with diffuse pattern of
inflammation.
Sites:
1. Orbit.
2. S.C. of hands & feet.
3. Pelvic soft tissue.

Prof. Dr. Ahmed Elrashedy

Pathology:
1. Widespread slowly formed & thinner pus (than in abscess).
2. Marked RBCs formation (Sanguineous).
Complications:
Systemic complications (through blood & lymphatic spread like those of
acute abscess) commonly occur.
Treatment: Medical in form of:
1. Antibiotics.
2. Anti-inflammatory drugs.

Acute Inflammation
Non - suppurative ( Aseptic)

1. Allergic inflammation: characterized by formation of excess eosinophils

(blood or / and tissue eosinophilia).
Examples: 1) Urticaria.
2) Bronchial asthma.
2. Catarrhal inflammation: characterized by formation of excess mucus.
Examples: in mucous surfaces.
1) Catarrhal rhinitis.
2) Catarrhal tonsillitis.

Prof. Dr. Ahmed Elrashedy

3. Serous inflammation: characterized by excess serous fluid.

Examples: 1) 2nd degree burn ( Vesicle formation).
2) Herpes zoster.
4. Fibrinous inflammation: characterized by excess fibrin threads.
Example: Lobar pneumonia.
5. Serofibrinous inflammation: characterized by excess serous fluid
& fibrin threads.
Examples: 1) Pleurisy.
2) Pericarditis.
3) Peritonitis.
6. Membranous inflammation: characterized by formation of a tight
membrane or pseudo-membrane that leave a raw oozing surface.
The membrane is formed of :
Living & dead bacteria.
Living & dead PNLs.
Necrotic tissue.
Fibrin threads.
Fluid exudate.
Example: 1) Diphtheria caused by Mycobacterium diphtheriae.
2) Bacillary dysentery caused by Shigella bacilli.

Prof. Dr. Ahmed Elrashedy

7. Hemorrhagic inflammation: characterized by excess RBCs due to

damage of the vessel wall.
Examples:
1) Anthrax.
2) Plaque.
8. Gangrenous (Necrotizing) inflammation: characterized by necrosis &
putrefaction by anaerobic bacteria.
Examples:
1) Gas gangrene.
2) Tetanus.

N.B.:
Tetany means carpo - pedal spasm due to hypocalcaemia as a result
of hypoparathyroidism.
Tetanus is an infective disease
characterized by necrosis &
putrefaction by Clostridium tetani.

Chronic Inflammation
Def.: A pathological condition characterized by persistence of the irritant
producing a progressive tissue damage together with a similar degree of
repair ( Fibrosis & regeneration ).
Characteristics:
1.Aggregation of chronic inflammatory cells forming a mass called granuloma.
2.The arterioles in the chronic inflammatory area showed thick wall & narrow
lumen ( End-arteritis obliterans= EAO).
3.The fluid exudate is scanty while the cellular exudate is abundant in chronic
inflammation.

Prof. Dr. Ahmed Elrashedy

Terminology
The term of inflammation ends by the suffix itis that is added to
the name of the affected organ.
The followings are examples of inflammation:
1. Encephalitis: inflammation of the brain tissue.
2. Meningitis: inflammation of the leptomeninges.
3. Dacryocystitis: inflammation of the lacrimal gland.
4. Blepharitis: inflammation of the eyelid.
5. Keratitis: inflammation of the cornea.
6. Iridocyclitis: inflammation of the iris & ciliary body.
7. Dermatitis: inflammation of the skin.
8. Rhinitis: inflammation of the nose.
9. Otitis media: inflammation of the middle ear.
10. Labyrinthitis: inflammation of the internal ear.
11. Glossitis: inflammation of the tongue.
12. Cheilitis: inflammation of the lips.
13. Stomatitis: inflammation of the mouth.

Prof. Dr. Ahmed Elrashedy

Terminology
14. Pneumonia: inflammation of the pulmonary alveoli.
15. Pneumonitis: inflammation of the lung interstitium.
16. Pleurisy: inflammation of the pleura.
17. Vasculitis: inflammation of an artery.
18. Phlebitis: inflammation of a vein.
19. Lymphangitis: inflammation of a lymph vessel.
20. Lymphadenitis: inflammation of a lymph node.
21. Gastritis: inflammation of the stomach.
22. Enteritis: inflammation of the small intestine.
23. Colitis: inflammation of the colon.
24.Proctitis: inflammation of the rectum.
25.Omphalitis: inflammation of the umbilicus.
26.Hepatitis: inflammation of the liver.

Prof. Dr. Ahmed Elrashedy

Terminology
27.Nephritis: inflammation of the renal tissue.
28.Pyelitis: inflammation of the renal pelvis.
29.Cystitis: inflammation of the urinary bladder.
30.Cholecystitis: inflammation of the gall bladder.
31.Cholangitis: inflammation of the bile duct.
32.Myometritis: inflammation of smooth muscle of uterus.
33.Endometritis: inflammation of lining epithelium of uterus.
34.Parametritis: inflammation of pelvic connective tissue.
35.Funnicultis: inflammation of the spermatic cord.
36.Orchitis: inflammation of the testis.
37.Palanitis: inflammation of the glans penis.
38.Salpingitis: inflammation of the Fallopian tube.
39.Synovitis: inflammation of the synovial membrane.

Prof. Dr. Ahmed Elrashedy

Terminology
40.Osteomyelitis: inflammation of bone cortex & marrow.
41.Dactylitis: inflammation of the terminal phalanx.
42.Onycolitis: inflammation of the nail bed.
43.Panniculitis: inflammation of the subcutaneous tissue.
44.Arthritis: inflammation of the joint.
45. Neuritis: inflammation of the nerve.
46.Osteitis: inflammation of the bone.
47.Chondritis: inflammation of the cartilage.
48.Tendenitis: inflammation of the tendon.
49.Fasciitis: inflammation of the fascia.
50.Myositis: inflammation of the muscles.
51.Parotitis: inflammation of the parotid gland.
52.Sialadenitis: inflammation of the salivary gland.
53.Cellulitis: acute diffuse suppurative inflammation.

Prof. Dr. Ahmed Elrashedy

Prof. Dr. Ahmed Elrashedy



Prof. Dr. Ahmed Elrashedy

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