بسم الله الرحمن الرحيم 1. INFLAMMATION DR:Gehan mohamed 2

الرحمن الله الرحمن بسم الله بسمالرحيمالرحيم

INFLAMMATIONINFLAMMATION

DR:Gehan mohamedDR:Gehan mohamed

Inflammation Definition:Definition: * *Inflammation is the local Inflammation is the local

vascular, lymphatic and cellular reactions vascular, lymphatic and cellular reactions of living tissue against an irritant. of living tissue against an irritant.

*Inflammation is a protective mechanism *Inflammation is a protective mechanism with the purpose of localization and with the purpose of localization and removal of the irritant. removal of the irritant.

*Inflammation is designated by adding *Inflammation is designated by adding the suffix the suffix ““itisitis”” to the English, Latin or to the English, Latin or Greek name of the organ affected e.g. Greek name of the organ affected e.g. tonsillitis, appendicitis, gastritis ... etc.tonsillitis, appendicitis, gastritis ... etc.

CAUSES OF INFLAMMATION

(1) Living Irritants: Bacteria and their toxins, viruses, parasites and fungi. (2) Non Living Irritants: include: (a) Physical irritants: e.g. excess heat, excess cold and radiations. (b) Chemical irritants: e.g. concentrated acids, alkalis, organic and inorganic poisons. (c) Mechanical irritants: e.g. trauma, mechanical friction and foreign bodies.

(3) Antigens: Cause allergic inflammation .

TYPES OF INFLAMMATIONTYPES OF INFLAMMATION

))11 ( (Acute InflammationAcute Inflammation:: Caused by an irritant of short duration .Caused by an irritant of short duration . The tissue response is rapid i.e. sudden The tissue response is rapid i.e. sudden

onset.onset. lasts for days to weeks.lasts for days to weeks. characterized by the presence of fluid characterized by the presence of fluid

exudates, fibrin threads and exudates, fibrin threads and polymorphonuclear leucocytes.polymorphonuclear leucocytes.

(2) Chronic Inflammation(2) Chronic Inflammation:: Caused by an irritant of prolonged action.Caused by an irritant of prolonged action. The tissue response is slow i.e. gradual onset.The tissue response is slow i.e. gradual onset. Inflammation lasts for months to years.Inflammation lasts for months to years. characterized by the presence of characterized by the presence of

macrophages, plasmamacrophages, plasma cells, lymphocytes and cells, lymphocytes and fibrosis. fibrosis.

(3) Subacute Inflammation(3) Subacute Inflammation:: Grades Grades between the acute and the chronic typesbetween the acute and the chronic types..

Acute InflammationAcute Inflammation

Pathogenesis of Acute Pathogenesis of Acute InflammationInflammation

The acute inflammatory reaction The acute inflammatory reaction consists of: consists of:

I. Local I. Local tissuetissue damage. damage. II. Local II. Local vascularvascular reactions. reactions. III. Local III. Local histiocyteshistiocytes reaction . reaction .

I. LOCALTISSUEI. LOCALTISSUE DAMAGEDAMAGE Occurs at the centre of the inflamed area Occurs at the centre of the inflamed area

with the maximum concentration of the with the maximum concentration of the irritant. Local death of tissue irritant. Local death of tissue (necrosis)(necrosis) will will result. result.

This local damage of cells together with This local damage of cells together with inflammatory stimulus trigger the release inflammatory stimulus trigger the release and activation of chemical substances and activation of chemical substances called called chemical mediatorschemical mediators as histamine, as histamine, serotonin and prostaglandins. serotonin and prostaglandins.

These chemical mediators play an important These chemical mediators play an important

role in promoting the vascular and cellular role in promoting the vascular and cellular changes in the inflamed area.changes in the inflamed area.

II. LOCAL VASCULAR REACTIONSII. LOCAL VASCULAR REACTIONS

(1)Transient vasoconstriction of the (1)Transient vasoconstriction of the small arteriolessmall arterioles:: Caused by the direct Caused by the direct effect of the irritant on the vascular wall. effect of the irritant on the vascular wall.

Vasoconstriction is a protective mechanism Vasoconstriction is a protective mechanism and lasts for seconds to minutes only. and lasts for seconds to minutes only.

(2)(2) Vasodilatation of the Blood Vasodilatation of the Blood VesselsVessels:: Occurs in the arterioles, Occurs in the arterioles, venules and capillaries due to: venules and capillaries due to: (a) Direct action of histamine on the (a) Direct action of histamine on the vascular wall. vascular wall. (b) Local axon reflex. (b) Local axon reflex.

The dilatation of the arterioles and The dilatation of the arterioles and capillaries will increase the blood flow capillaries will increase the blood flow & is called hyperaemia. The inflamed & is called hyperaemia. The inflamed area becomes red and hot. area becomes red and hot.

(3)(3) SlowingSlowing of the Blood Stream of the Blood Stream

(Stasis):(Stasis): Caused by:Caused by:

(a)(a) Increased viscosity of the blood due to Increased viscosity of the blood due to formation inflammatory fluid exudates. formation inflammatory fluid exudates. This is the main cause of stasis. This is the main cause of stasis.

(b) Histamine causes swelling of the (b) Histamine causes swelling of the vascular endothelium which become vascular endothelium which become sticky and offer mechanical resistance sticky and offer mechanical resistance to the blood.to the blood.

(c) Most of the capillaries in the (c) Most of the capillaries in the inflamed area open and blood inflamed area open and blood reaching the arterioles will be reaching the arterioles will be distributed among large distributed among large number of capillaries, so number of capillaries, so slowing occurs.slowing occurs.

(4) Formation of the Inflammatory (4) Formation of the Inflammatory Exudates: Exudates:

The intravascular contents (plasma The intravascular contents (plasma and cells) escape into the interstitial and cells) escape into the interstitial tissue spaces forming the tissue spaces forming the inflammatory exudates which consists inflammatory exudates which consists of a fluid component and a cellular of a fluid component and a cellular component. component.

(5) Dilatation of lymphatic vessels:(5) Dilatation of lymphatic vessels:

to accelerate the lymph flow and to accelerate the lymph flow and drains the fluid exudates.drains the fluid exudates. 1414

A-The Inflammatory Fluid ExudatesA-The Inflammatory Fluid Exudates

Mechanism of formation:Mechanism of formation: (1)(1) Increased capillary permeability to Increased capillary permeability to

plasma and its proteins caused by plasma and its proteins caused by histamine (the main cause). histamine (the main cause).

(2) Increased capillary hydrostatic (2) Increased capillary hydrostatic pressure due to dilatation of the pressure due to dilatation of the arterioles and increased blood flow. arterioles and increased blood flow. This pushes fluids outside the This pushes fluids outside the capillaries. capillaries.

(3) Increased osmotic pressure (3) Increased osmotic pressure of the of the interstitial tissue fluid as the large interstitial tissue fluid as the large protein molecules split into smaller protein molecules split into smaller ones in the process of tissue necrosis. ones in the process of tissue necrosis. This acts as a suction force from the This acts as a suction force from the capillaries. capillaries.

Characters:Characters:

- - High protein content, 4-8 gm% (the normal High protein content, 4-8 gm% (the normal interstitial tissue fluid contains 1 gm% interstitial tissue fluid contains 1 gm% protein). protein).

- High fibrinogen content (turbid & clots on - High fibrinogen content (turbid & clots on standing). standing).

- High specific gravity (above 1018). - High specific gravity (above 1018).

- High cellular content (polymorphs & - High cellular content (polymorphs & macrophages)macrophages)

Functions: Functions:

(1) It dilutes toxins, chemicals and (1) It dilutes toxins, chemicals and poisons, so minimizes their effects. poisons, so minimizes their effects.

(2) Brings antibodies from the blood to (2) Brings antibodies from the blood to the site of inflammation. the site of inflammation.

(3) Supplies nutrition for the cells and (3) Supplies nutrition for the cells and carries away waste products. carries away waste products.

(4) Fibrinogen forms a fibrin (4) Fibrinogen forms a fibrin network, which acts as a network, which acts as a mechanical barrier to the spread mechanical barrier to the spread of infection and as a bridge for of infection and as a bridge for leucocytes to reach the irritant.leucocytes to reach the irritant.

B- The inflammatory cellular B- The inflammatory cellular exudatesexudates

1- 1- Margination of leucocytesMargination of leucocytes:: TheThe polymorphs leave the axial blood stream polymorphs leave the axial blood stream

due to stasis and settle on the due to stasis and settle on the endothelial lining of the capillaries.endothelial lining of the capillaries.

2- 2- Emigration of leucocytesEmigration of leucocytes:: The The polymorphs push their ways between the polymorphs push their ways between the swollen endothelial cells through the swollen endothelial cells through the widened pores by means of pseudopodia widened pores by means of pseudopodia to outside the vessels by amoeboid to outside the vessels by amoeboid movement.movement.

3- 3- Emigration of blood monocytesEmigration of blood monocytes:: which which change in the inflamed area to change in the inflamed area to macrophages together with the tissue macrophages together with the tissue histiocytes.histiocytes.

4- 4- ChemotaxisChemotaxis:: Is the directed movement Is the directed movement of polymorphs and macrophages in the of polymorphs and macrophages in the area of inflammation towards the area of inflammation towards the irritant. This is helped by chemical irritant. This is helped by chemical products produced by polymorphs. The products produced by polymorphs. The inflammatory cells move on fibrin inflammatory cells move on fibrin threads.threads.

5-5- Phagocytosis Phagocytosis:: It is the ingestion It is the ingestion and destruction of bacteria, and destruction of bacteria, necrotic debris and foreign necrotic debris and foreign particles by phagocytic particles by phagocytic inflammatory cells (polymorphs inflammatory cells (polymorphs and macrophages).and macrophages).

III. LOCAL REACTION OF TISSUE III. LOCAL REACTION OF TISSUE HISTIOCYTESHISTIOCYTES

Late in acute inflammation the Late in acute inflammation the macrophages replace the polymorphs.macrophages replace the polymorphs.

Macrophages are derived from tissue Macrophages are derived from tissue histiocytes and blood monocytes. histiocytes and blood monocytes. They phagocytose dead bacteria, They phagocytose dead bacteria, necrotic debris, pus cells and fibrin necrotic debris, pus cells and fibrin threads cleaning the area of threads cleaning the area of inflammation and preparing the tissue inflammation and preparing the tissue for the repair process. for the repair process.

CARDINAL SIGNS AND SYMPTOMS OF CARDINAL SIGNS AND SYMPTOMS OF ACUTE INFLAMMATIONACUTE INFLAMMATION

))11 ( (Redness:Redness: Caused by vasodilatation Caused by vasodilatation of the capillaries. of the capillaries. (2) Hotness:(2) Hotness: Caused by arteriolar Caused by arteriolar dilatation and increased blood flow. dilatation and increased blood flow. (3) Swelling:(3) Swelling: Caused by the vascular Caused by the vascular dilatation and the accumulation of the dilatation and the accumulation of the inflammatory fluid and cellular exudate. inflammatory fluid and cellular exudate.

(4) Pain:(4) Pain: Caused by irritation of the Caused by irritation of the nerve endings by toxins and Pressure of nerve endings by toxins and Pressure of the inflammatory exudate on the the inflammatory exudate on the sensory nerves. sensory nerves. (5) (5) Loss of function:Loss of function: due to due to destruction of tissues or to avoid Paindestruction of tissues or to avoid Pain . .

General Effects Of Acute General Effects Of Acute InflammationInflammation

(1) Leucocytosis(1) Leucocytosis:: Increase in the Increase in the number of polymorphonuclear number of polymorphonuclear leucocytes in the blood above leucocytes in the blood above l0000/cml0000/cm33. Leucocytosis is caused by . Leucocytosis is caused by the liberation of the liberation of ““leucocytosis leucocytosis promoting factorpromoting factor”” from the injured from the injured tissue which stimulates the bone tissue which stimulates the bone marrow to produce more leucocytes.marrow to produce more leucocytes.

(2) Fever (Pyrexia):(2) Fever (Pyrexia): Due to the Due to the release of Pyrogenic substances from release of Pyrogenic substances from the bacteria and dead leucocytes. the bacteria and dead leucocytes. Pyrogenic substances disturb the Pyrogenic substances disturb the function of the heat regulating centre function of the heat regulating centre in the hypothalamus causing fever. in the hypothalamus causing fever. Fever disturbs the vitality of bacteria, Fever disturbs the vitality of bacteria, but is also harmful to the body as it but is also harmful to the body as it causes loss of fluids and electrolytes.causes loss of fluids and electrolytes.

(3) Toxic effects(3) Toxic effects:: as anorexia, as anorexia, headache and degeneration in headache and degeneration in parenchymatous organs.parenchymatous organs.

FATE OF ACUTE INFLAMMATIONFATE OF ACUTE INFLAMMATION

(1) Resolution:(1) Resolution: Means complete restoration of the Means complete restoration of the

inflamed area to normal. It occurs inflamed area to normal. It occurs when tissue damage is minimal. The when tissue damage is minimal. The products of inflammation are rapidly products of inflammation are rapidly removed. Resolution is the usual removed. Resolution is the usual course of acute inflammation caused course of acute inflammation caused by mild chemical or physical irritant, by mild chemical or physical irritant, many viral infections and lobar many viral infections and lobar pneumonia. pneumonia.

(2) Regression and Healing:(2) Regression and Healing: The body defense overcomes the The body defense overcomes the

irritant. Part of the necrotic tissue, irritant. Part of the necrotic tissue, dead cells and fibrin are removed by dead cells and fibrin are removed by the macrophages. The rest gets the macrophages. The rest gets liquefied. liquefied.

The liquefied part together with the The liquefied part together with the fluid exudates are drained by the fluid exudates are drained by the lymphatics and veins. Next healing lymphatics and veins. Next healing occurs by fibrosis. occurs by fibrosis.

(3) Progression and Spread:(3) Progression and Spread: The bacteria overcome the defense The bacteria overcome the defense

mechanism and inflammation spreads mechanism and inflammation spreads directly, by lymphatics and by blood directly, by lymphatics and by blood causing toxaemia, bacteraemia, causing toxaemia, bacteraemia, septicaemia or pyaemia. septicaemia or pyaemia.

(4) Chronicity:(4) Chronicity: The causative agent is partially The causative agent is partially

overcomed, but the body is unable to get overcomed, but the body is unable to get rid of it completely. It remains as a weak rid of it completely. It remains as a weak irritant acting on the tissue for a long time.irritant acting on the tissue for a long time.

SuppurativeSuppurative– LocalizedLocalized

AbscessAbscess FuruncleFuruncle CarbuncleCarbuncle

– DiffuseDiffuse Cellulitis Cellulitis

Non-Non-suppurativesuppurative– CatarrhalCatarrhal– MembranousMembranous– AllergicAllergic– FibrinousFibrinous– Sero-fibrinousSero-fibrinous– HemorrhagicHemorrhagic– NecrotizingNecrotizing

Types of acute inflammation

I. SUPPURATIVE INFLAMMATION I. SUPPURATIVE INFLAMMATION (Pyogenic or Septic)(Pyogenic or Septic)

Definition:Definition: Severe acute inflammation Severe acute inflammation characterized by pus formationcharacterized by pus formation

Causes:Causes: Pyogenic microorganisms as Pyogenic microorganisms as staphylococcus aureus, staphylococcus aureus, pneumococcus, gonococcus and pneumococcus, gonococcus and bacillus coli. bacillus coli.

Abscess

Definition:Definition: Localized suppurative Localized suppurative inflammation resulting in the inflammation resulting in the formation of an irregular cavity formation of an irregular cavity filled with pusfilled with pus

Etiology:Etiology: Caused mainly by Caused mainly by staphylococcus aureus which staphylococcus aureus which produce coagulase enzyme that produce coagulase enzyme that helps fibrin formation and localize helps fibrin formation and localize the infection.the infection.

Sites:Sites:Commonly the abscess Commonly the abscess occurs in in the occurs in in the subcutaneous tissue and subcutaneous tissue and in any organ as the lung, in any organ as the lung, brain, liver, breast. brain, liver, breast.

Characters:Characters: the abscess shows three zones. the abscess shows three zones.

(a) Central zone of necrosis.(a) Central zone of necrosis.(b) Midzone containing pus.(b) Midzone containing pus.(c) Peripheral zone of inflamed tissue (c) Peripheral zone of inflamed tissue called called pyogenic membrane.pyogenic membrane.

Complications:Complications:– Lymphangitis and lymphadenitisLymphangitis and lymphadenitis– Septicemia, bacteremia and Septicemia, bacteremia and

toxemiatoxemia– Septic thrombophlebitis and Septic thrombophlebitis and

payemic abscessespayemic abscesses– ChronicityChronicity

CellulitisCellulitis Definition:Definition: Acute diffuse Acute diffuse

suppurative inflammation.suppurative inflammation. Cause:Cause: Streptococcus haemolyticus. Streptococcus haemolyticus.

The organism produces two enzymes:The organism produces two enzymes:

(1) (1) Fibrinolysin (streptokinase): Fibrinolysin (streptokinase): Dissolves fibrin.Dissolves fibrin. (2) (2) Hyaluronidase (spreading factor): Hyaluronidase (spreading factor): Dissolves hyaluronic acid of ground Dissolves hyaluronic acid of ground substance helping spread of bacteria substance helping spread of bacteria and its toxins. and its toxins.

Sites:Sites: Loose connective tissue as Loose connective tissue as subcutaneous tissue, scrotum, upper subcutaneous tissue, scrotum, upper respiratory tract and wall of the respiratory tract and wall of the appendix.appendix.

Characters:Characters: ((1)1) Failure of localization because of Failure of localization because of

absence of fibrin. absence of fibrin. (2) Extensive necrosis.(2) Extensive necrosis.(3) Pus is thin in consistency and may (3) Pus is thin in consistency and may contain many red cells i.e. sanguinous.contain many red cells i.e. sanguinous.

Complications:Complications: (1) Acute lymphangitis and (1) Acute lymphangitis and

lymphadenitis. lymphadenitis. (2) Septic thrombophlebitis (2) Septic thrombophlebitis

causing pyaemic abscesses.causing pyaemic abscesses. (3) Septicaemia.(3) Septicaemia.

II.II. NON-SUPPURATIVENON-SUPPURATIVE INFLAMMATIONINFLAMMATION

11 . .Catarrhal Inflammation:Catarrhal Inflammation: Mild acute inflammation of the Mild acute inflammation of the mucous membranes of the mucous membranes of the respiratory and GIT characterized respiratory and GIT characterized by excess mucus secretion e.g. by excess mucus secretion e.g. catarrhal rhinitis (common cold), catarrhal rhinitis (common cold), bronchitis, ... etcbronchitis, ... etc . .

2. Membranous Inflammation 2. Membranous Inflammation (Pseudomembranous) (Pseudomembranous)

Severe acute inflammation Severe acute inflammation characterized by the formation of a characterized by the formation of a pseudomembrane on the affected pseudomembrane on the affected surface formed of necrotic cells, fibrin surface formed of necrotic cells, fibrin threads, leucocytes and the threads, leucocytes and the causative organism e.g. diphtheria causative organism e.g. diphtheria and bacillary dysentery.and bacillary dysentery.

PathogenesisPathogenesis:: The bacteria remain on the mucosal The bacteria remain on the mucosal

surface and produce powerful exotoxin surface and produce powerful exotoxin which causes patchy mucosal necrosis. which causes patchy mucosal necrosis. The exotoxin diffuses through the The exotoxin diffuses through the necrotic mucosa to the submucosa necrotic mucosa to the submucosa causing acute inflammation. The causing acute inflammation. The exotoxin is absorbed in the blood stream exotoxin is absorbed in the blood stream causing severe toxaemia. causing severe toxaemia.

A yellowish white slightly elevated A yellowish white slightly elevated pseudomembrane is formed on the pseudomembrane is formed on the surface. The membrane is adherent and surface. The membrane is adherent and its removal leaves a bleeding surface its removal leaves a bleeding surface with the formation of another membrane. with the formation of another membrane.

3. Fibrinous3. Fibrinous Inflammation:Inflammation: Characterized by an exudate rich in Characterized by an exudate rich in fibrinogen e.g. lobar pneumonia.fibrinogen e.g. lobar pneumonia.

4. Serofibrinous4. Serofibrinous Inflammation:Inflammation: It involves serous sacs as pleura, It involves serous sacs as pleura, peritoneum and pericardium. peritoneum and pericardium. Characterized by excess serous Characterized by excess serous exudates in the sac and deposition of exudates in the sac and deposition of fibrin on the surface. fibrin on the surface.

5. Haemorrhagic Inflammation:5. Haemorrhagic Inflammation:Characterized by cellular exudate Characterized by cellular exudate rich in the red blood cells due to rich in the red blood cells due to vascular damage e.g. smallpox vascular damage e.g. smallpox and haemolytic streptococcal and haemolytic streptococcal infection. infection.

6. Necrotizing Inflammation:6. Necrotizing Inflammation: AcuteAcute inflammation characterized inflammation characterized by markedby marked tissue necrosis. tissue necrosis.

7. 7. Allergic Inflammation:Allergic Inflammation:

as urticaria. It is an antigen antibody as urticaria. It is an antigen antibody reaction characterized by abundant reaction characterized by abundant fluid exudates and eosinophils.fluid exudates and eosinophils.

CHRONIC INFLAMMATIONCHRONIC INFLAMMATION Chronic inflammation is Chronic inflammation is

characterized by the following:characterized by the following: (1) The irritant is mild and has a (1) The irritant is mild and has a prolonged action. prolonged action. (2) Chronic inflammation may follow (2) Chronic inflammation may follow acute inflammation or starts as slowly acute inflammation or starts as slowly progressing chronic disease as in progressing chronic disease as in tuberculosis and syphilis. tuberculosis and syphilis. (3) The tissue response is gradual and (3) The tissue response is gradual and prolonged. prolonged.

(4) (4) The small arteries and arterioles The small arteries and arterioles show thickening and narrowing called show thickening and narrowing called end arteritis obliterans. end arteritis obliterans. (5) The inflammatory fluid exudates (5) The inflammatory fluid exudates is scanty. is scanty. (6) The inflammatory cellular (6) The inflammatory cellular exudates consists of exudates consists of lymphocytes, lymphocytes, plasma cells, macrophages and plasma cells, macrophages and foreign-body giant cellsforeign-body giant cells..

TypesTypes of Chronic inflammationof Chronic inflammation:: (1) (1) Chronic non-specificChronic non-specific

inflammation:inflammation: Different irritants Different irritants produce inflammatory reactions of produce inflammatory reactions of the same microscopic picture e.g. the same microscopic picture e.g. chronic abscess and chronic tonsillitis.chronic abscess and chronic tonsillitis.

(2) (2) Chronic specificChronic specific inflammation:inflammation: Each irritant or organism produces a Each irritant or organism produces a characteristic microscopic picture characteristic microscopic picture called granuloma e.g. tuberculosis, called granuloma e.g. tuberculosis, bilharziasis and leprosy bilharziasis and leprosy

Differences between acute Differences between acute and and

chronic chronic inflammationinflammation

ItemItemAcute inflammationAcute inflammationChronic inflammationChronic inflammation

OnsetOnsetRapid and suddenRapid and suddenSlow and gradualSlow and gradual

DurationDurationShortShortProlongedProlonged

Vascular Vascular phenomenaphenomena

PresentPresentSlight or absentSlight or absent

Cardinal signsCardinal signsPresentPresentSlight or absentSlight or absent

Mic. ChangesMic. ChangesCellsCells

Blood vesselsBlood vessels

-Polymorphs, pus cells, -Polymorphs, pus cells, macrophagesmacrophages

-Numerous, thin walled, -Numerous, thin walled, dilated and filled with dilated and filled with bloodblood

-Plasma cells, -Plasma cells, lymphocytes, lymphocytes, macrophages, giant macrophages, giant cells, fibroblastscells, fibroblasts

-Few thick walled -Few thick walled narrow lumen(end narrow lumen(end arteritis oblitrans)arteritis oblitrans)

GranulomaGranuloma

– DefinitionDefinition::

–Chronic specific inflammation Chronic specific inflammation characterized by focal characterized by focal accumulation of large number accumulation of large number of chronic inflammatory cells of chronic inflammatory cells to form tumor like massto form tumor like mass. .

TypesTypes(1)Infective granuloma(1)Infective granuloma

1.1.Bacterial as TB, leprosy & syphilisBacterial as TB, leprosy & syphilis

2.2.Parasitic as bilharziasis & Parasitic as bilharziasis & leishmaniasisleishmaniasis

3.3.Mycotic (fungus) as madura foot, Mycotic (fungus) as madura foot, actinomycosisactinomycosis

4.4.Viral as granuloma inguinaleViral as granuloma inguinale

(2)Non-infective granuloma(2)Non-infective granuloma As silicosis, asbestosis and As silicosis, asbestosis and foreign-body granuloma.foreign-body granuloma.

(3) Unknown cause(3) Unknown cause

sarcoidosis, crohns diseasesarcoidosis, crohns disease 6969

Histopathology of Histopathology of granulomagranuloma

A- Macrophages main bulk of A- Macrophages main bulk of granuloma, made of tissue histiocytes, granuloma, made of tissue histiocytes, blood monocytes and foreign body blood monocytes and foreign body giant cellsgiant cells

B- Other inflammatory cells as B- Other inflammatory cells as lymphocytes, plasma cells, eosinophils.lymphocytes, plasma cells, eosinophils.

C- Granulation tissueC- Granulation tissue D- Fibrous tissueD- Fibrous tissue E- Specific organism or foreign bodyE- Specific organism or foreign body

Schistosomiasis

Leishmaniasis

Leprosy

Sarcoidosis

بسم الله الرحمن الرحيم 1. INFLAMMATION DR:Gehan mohamed 2

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