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Inflammation
PresentedBy
Ahmed El-RashedyProfessor & Previous Head
of Pathology DepartmentAl-Azhar University
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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.
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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.
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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.
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ChronicAcute
GradualSudden1. Onset
Mild.Severe.2. Irritant
Longer (months-years)Short ( days- weeks)3. Duration
Slowly progressiveRapidly progressive4. Course
LittleExcess
ExcessModerate
5. Exudate:
A) Fluid part.B) Cellular part
Plasma cells.
Lymphocytes.
Macrophages(Histiocytes).
Giant cells.
Fibroblasts.Eosinophils.
Polymorphs (Neutrophils).
Pus cells ( Dead polymorphs).
RBCs.
Macrophages.
Eosinophils.
6. Types of cells
From tissue histiocytes.From blood monocytes.7. Origin of
macrophages
Perivascular or diffuse.Diffuse.8. Arrangement
Marked.Mild.9. Vascular changes
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ChronicAcute
Little congested , narrow
lumen & thick - walled
( End-arteritis obliterans).
Congested, dilated & thin-
walled
10. Blood vessels
Associate.Follow.11.Repair
PresentAbsent12.Granulation tissue
Marked.Absent13.Fibrosis
Mild.Severe.14.Toxemia
Absent except swelling.Redness hotness
pain swelling loss of
function.
15.CardinalSigns
usually absent. Totalleucocytic count is normal
or decrease
present.16.General changes asfever and leucocytosis
Specific or non - specific.Suppurative or non sup.17.Types
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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: asBradykinin & 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).
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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.
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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 theaction 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: Passiveescape 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.
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Inflammatory Exudate: Two components
1. Fluid exudate.
2. Cellular exudate. Cellular exudateFluid 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.
High protein (4-8 gm %).
High specific gravity
>1018.
High fibrinogen.
1. Composition:
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Cellular exudateFluid exudate
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 lysosomalenzymes 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.
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 PNLstraverse.
3. Helps the repair which
starts early at the site of
fibrin.
2. Function:
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Cellular exudateFluid exudate
5. Lymphocytes:
They function in both humoral (B-cells) & incell-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.
2. Function:
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Differences Between Exudate and
TransudateTransudateExudateLow ( < 3 gm % )High ( > 3 gm % )1. Protein content
LowHigh2. Fibrinogen contentHypocellular
(Poor in cells)
Hypercellular
(rich in cells)
3. Cellular content
< 1018> 10184. Specific gravity
AbsentPresent5.Coagulation on standing
Interstitial fluid
or serous fluid
Plasma6. Origin
Oedema & CVCInflammation7. Example
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I) AbscessPathology: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 necrotictissue).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.
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I) AbscessFate :
Due to the increased osmotic pressure inside the abscess, fluid is dragged
from the surroundings with increased tension within the abscess causingsevere 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.
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I) AbscessB) 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 bloodstream 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.
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Differences Between Acute & Chronic
Abscess
Chronic abscessAcute abscess
Regular & smoothIrregular & shreddy1. Wall
Little thick pusProfuse thin pus2. Content
Chronic inflammatory cellsAcute inflammatory cells3. Cell type
By excisionBy incision4. Treatment
May occurAbsent5. Calcification
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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) CarbuncleDef.: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 ofinflammation.
Sites:
1. Orbit.
2. S.C. of hands & feet.
3. Pelvicsoft tissue.
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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 InflammationNon - 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.
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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 tightmembrane 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.
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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 InflammationDef.: 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.
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TerminologyThe term of inflammation ends by the suffix itisthat 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.
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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.
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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.
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P f D Ah d El h d
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Prof. Dr. Ahmed Elrashedy
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