1. DR .HALA BADAWI LECTURER OF PATHOLOGY
Inflammation
DR .HALA BADAWI
LECTURER OF PATHOLOGY

2. INFLAMMATION DEFINITION:
Inflammation is the reaction of vascularized living tissue to local injury. It is a series of vascular and cellular reactions aiming to protect the body against the injurious agent .
TYPES:
-Acute: sudden onset and short duration ( hours - days)
-Chronic: gradual onset and long duration ( days -years)

3. INFLAMMATION CAUSES: Living irritants
Bacteria, viruses, parasites and fungi
Non-living irritants
Physical, chemical and mechanical
Antigens

4. ACUTE INFLAMMATION Caused by an irritant of short duration of action
The tissue response is rapid i.e. sudden onset
Inflammation lasts for days or weeks
Characterized by presence of fluid exudate and cellular exudate mainly polymorph-nuclear leucocytes

5. CARDINAL SIGNS AND SYMPTOMS OF ACUTE INFLAMMATION
REDNESS
HOTNESS
SWELLING
PAIN
LOSS OF FUNCTION

6. Major events in inflammation
Cellular events
Vascular events
Vasodilatation of arterioles and capillaries
Increased blood flow
Slowing of blood stream
Increased capillary permeability
Margination of leucocytes
Emigration of leucocytes
Emigration of monocytes
Chemotaxis:
(directed movement towards area of inflammation)
Phagocytosis:
(engulfment of bacteria and necrotic tissue)
Formation of
Inflammatory
Fluid exudate

7. Vascular Events in inflammation
Vasodilatation of arterioles and capillaries
Increased blood flow
Slowing of blood stream
Increased capillary permeability

8. Cellular Events in inflammation
Margination , Emigration of neutrophils & monocytes
Chemotaxis & phagocytosis

9. Phagocytosis,
Killing &
degradation

10. Chemical Mediator of Inflammation

11. CHEMICAL MEDIATORS ACTIONS Bind to specific receptors on the cells
Histamine
Prostaglandins
C3a & C5a
Vasodilatation
Increase vascular permeability
Histamine, kinins, leukotriens
Chemotaxis
Leukotriens & lysosomal components

12. The Inflammatory Fluid Exudate
Function:
It dilutes bacterial toxins and chemical irritants.
It brings antibodies to the area of inflammation.
It brings the chemical mediators derived from plasma to the area.
It contains fibrinogen which changes to fibrin by activation of clotting system. Fibrin helps in localization of inflammation by surrounding the area .
Fate:
Fluid exudate is absorbed by lymphatics.

14. Fate of Acute inflammation
Complete resolution
Healing by scarring
Progression and spread:
(direct, lymphatic & blood spread)
Chronicity

15. TYPES OF ACUTE INFLAMMATION
SUPPURATIVE
INFLAMMATION
NON-SUPPURATIVE
INFLAMMATION

16. I- SUPPURATIVE INFLAMMATION
Types:
II- Diffuse Supp. Inflamm.
Cellulitis,
Suppurative appendicitis,
Suppurative cholecystitis,
Suppurative peritonitis,
Suppurative meningitis
…etc.
I-Localized
Supp. Inflamm.
Abscess,
furuncle,
carbuncle

17. I- LOCALIZED SUPPURATIVE INFLAMMATION
Abscess
carbuncle
furuncle

18. Abscess Definition: Cavity containing pus
(pus is formed of fluid exudate, fibrin,pus cells, polymprph, macrophages, necrotic tissue and bacteria)

19. Abscess Fate of abscess: Small abscess:
Pus may be absorbed followed by healing
Large abscess:
Should be evacuated, spontaneous or surgical

20. Abscess Complication of abscess: Ulcer (local defect on the surface)
Sinus (blind end tract) & Fistula (tract with two openings)
Hemorrhage & gangrene
Spread of infection
Ulcer
Sinus
Gangrene

21. II- DIFFUSE SUPPURATIVE INFLAMMATION
Acute supp. appendicitis
Suppurative meningitis
Diffuse sup.cholecystitis
Cellulitis
Cellulitis

22. NON-SUPPURATIVE INFLAMMATION
Catarrhal inflammation: e.g.common cold
Pseudo-membranous inflam.: e.g.diphtheria
Fibrinous inflammation: e.g. fibrinous pericarditis, fibrinous pleurisy, fibrinous peritonitis.
Serous inflammation: e.g. burns
Haemorrhagic inflammation
Gangrenous (necrotizing) inflammation
Allergic inflammation

23. NON-SUPPURATIVE INFLAMMATION
Fibrinous pericarditis
Fibrinous pleurisy
Fibrinous pericarditis
Gangrenous inflammation
Haemorhagic pericarditis.
Fibrinous peritonitis

24. CHRONIC INFLAMMATION Characterized by:
Mild irritant with a prolonged action
Tissue response is gradual and prolonged (mild vascular dilatation and congestion)
Tissue destruction is progressive and gradually replaced by fibrous tissue with thickening and narrowing of blood vessels (endarteritis obliterans)
Scanty fluid exudate

25. Chronic Inflammatory Cellular Exudate
Composed of:
Lymphocytes
Plasma cells
Macrophages
Giant cells
Esinophils in parasitic and allergic inflammation.

26. Types of Chronic Inflammation
1- Chronic non-specific inflammation
Different irritants produce inflammatory reaction of the same microscopic picture
2- Chronic specific inflammation
Each irritant produces inflammation of a characteristic microscopic picture

27. Chronic non-specific inflammation

28. Granuloma Definition:
A type of chronic inflammation characterized by focal accumulation of large number of macrophages together with lymphocytes, plasma cells, giant cells and fibroblasts forming tiny granules

29. Types of Granulomas 1-Infective granuloma
a. Bacterial e.g.TB, leprosy & syphilis
b. Parasitic e.g. Bilharziasis
c. Fungal e.g. madura foot
2-Non-infective granuloma
a. Silicosis and asbestosis
b. Foreign body granuloma
3-Granuloma of unknown cause
Sarcoidosis

30. Tuberculous granuloma of the lung