inflammation dr. elrashedy.pdf

8/10/2019 inflammation dr. elrashedy.pdf

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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.

Prof.Dr.AhmedElrashedy


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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.

Prof.Dr.Ahm

edElrashedy


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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.

Prof. Dr. Ahmed Elrashedy


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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.


P f D Ah d El h d


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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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Prof Dr Ahmed Elrashedy


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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.

Prof.Dr.A

hmedElrashedy


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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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