1. By Dr. Ghada Ahmed Lecturer of pathology Benha Faculty of Medicine

2. Part I Objectives 1- Define inflammation
2- Classify types of inflammation
3- Explain mechanism of acute inflammation
4- Enumerate the cardinal signs of acute inflammation

3. Definition Irritant Reaction of living tissue Aims to:
1- prevent tissue damage
2- localization of irritant
3- destruction of irritant
4- preparing for repair
lymphatic
cellular
vascular
Irritant

4. Irritant (types & effects)

5. Inflammation
Acute
Subacute
Chronic

6. Acute inflammation Mild/ severe irritant Short duration
Rapid tissue response
Acute inflammation

7. Cardinal signs of inflammation

8. Mechanism of acute inflammation
Local changes
1- Tissue destruction
2- Vascular phenomenon
3- Rx of tissue histiocytes
General changes
1- changes in blood cells
6- degenerative changes
7- septicemia
5-hyperplasia of draining LN
4- liver secretes proteins
3- loss of appetite
2- fever
8- pyemia

9. 1- Local tissue destruction
Injurious agent
Chemical mediators
Local tissue destruction

10. 2. Local Vascular phenomenon Dilatation of lymphatic vessels
Transient VC VD
Stasis
Inflammatory exudate
Dilatation of lymphatic vessels

11. Fluid exudate: = inflammatory extravascular fluid capillary HP cap permeability tissue OP
Cellularity
Sp gravity
Protein content
(fibrinogen- clot)

12. Fluid exudate

13. Function of fluid exudate
Formation of fibrin network
Dilutes bacterial toxins
Brings antibodies to destruct irritant

14. N.B: Chemotaxis & Phagocytosis
Inflammatory exudate
Cellular
Margination
Migration
Activation
Diapedesis
Fluid
N.B: Chemotaxis & Phagocytosis

15. Cellular exudate

16. Function of cellular exudate
PNLs enzymes
attak, phagocytose, kill the organism
Later : phagocytosis by macrophages

17. Attraction of leucocytes towards the irritant by chemotactic factors
Chemotaxis
Attraction of leucocytes towards the irritant by chemotactic factors

18. Phagocytosis
Ingestion and destruction of foreign body and bacteria by phagocytic cells

19. 2. Local Vascular phenomenon Dilatation of lymphatic vessels
Transient VC VD
Stasis
Inflammatory exudate
Dilatation of lymphatic vessels

20. 3. Local reaction of tissue hiseocytes
By macrophages:
Proliferate
Phagocytosis: dead bacteria, necrotic debris
Clean the area of inflammation

21. Part II Objectives 1- Explain mechanism of acute inflammation
2- Define chemical mediators and discuss their role in acute inflammation
3- Discuss the fate of acute inflammation
4- Classify then discuss types of acute inflammation

22. Mechanism of acute inflammation
Local changes
1- Tissue destruction
2- Vascular phenomenon
3- Rx of tissue histiocytes
General changes
1- changes in blood cells
6- degenerative changes
7- septicemia
5-hyperplasia of draining LN
4- liver secretes proteins
3- loss of appetite
2- fever
8- pyemia

23. Cells of Acute inflammation
PNLs
Macrophages
RBCs
Pus cells

24. Chemical mediators of acute inflammation
Chemical factors derived from plasma and cells (e.g. PNLs, monocytes, endoth cs, macrophages, fibroblasts)
Found as precursors in inactive forms.
Inflammatory stimulus triggers their release, activation, de novo synthesis
Act by binding to specific receptors on target cells

25. Chemical mediators of acute inflammation
Examples:
PGs: VD, fever, pain
Histamine, serotonin: increased permeability
C5a: increased permeability, chemotaxis
Cytokines: chemotaxis, leukocyte activation
Lysosomal enz of PNLs & macrophages: tissue damage

26. Fate of acute inflammation
Resolution
Spread
Chronicity

27. Quiz Mark TRUE or FALSE:
1- Histamine release causes increased capillary permeability.
2- Diapedesis is an energy-dependent process.
3- Acute inflammation is a rapid tissue response against severe irritants only.
4- Opsonization is covering leucocytes with opsonin to target it for phagocytosis.

28. Acute inflammation
Suppurative
Localized
Diffuse
Non-suppurative

29. Suppurative inflammation
Definition:
Acute inflammation chch by PUS formation
Cause:
Pyogenic organism (staph, strept,……)

30. Suppurative inflammation
Chch of pus
Composition of pus

31. Localizes suppurative inflammation (Abscess )
Definition
Sites
Cause

32. Pathogenesis of abscess

33. Pathogenesis of abscess
opening
Cavity containing pus
Pyogenic membrane

34. Complications of abscess
Chronicity
Spread
Complications of healing

35. Complications of abscess healing
keloid

36. Furuncle (boil)
Carbuncle
Diabetes

37. Diffuse suppurative inflammation
Cellulitis
Definition
Sites
Cause
Differs from abscess….

38. Complications of diffuse suppurative inflammation
Spread
Acute Lymphangitis
Acute Lymphadenitis
Thrombophlebitis
Septicaemia

39. Non-suppurative inflammation
Types: (according to features of exudate)
1- Catarrhal infl.
2- Membranous infl.
3- Fibrinous
4- Serous
5- Serofibrinous infl.
6- Hemorrhagic
7- Necrotizing
8- Allergic

40. Catarrhal inflammation
Definition:
Sites
Morphology
Fate

41. Catarrhal inflammation

42. Membranous (pseudomembranous) inflammation
Definition
Examples
Pathogenesis
Morphology
Complications
Exotoxin

43. Membranous (pseudomembranous) inflammation

44. Part III Objectives
1- classify then discuss types of acute inflammation
2- define chronic inflammation, its causes, features and types
3- compare between acute and chronic inflammation

45. Non-suppurative inflammation
Types: (according to features of exudate)
1- Catarrhal infl.
2- Membranous infl.
3- Fibrinous
4- Serous
5- Serofibrinous infl.
6- Hemorrhagic
7- Necrotizing
8- Allergic

46. Fibrinous inflammation
Serous inflammation
Serofibrinous inflammation

47. Serofibrinous inflammation

48. Serofibrinous inflammation

49. Hemorrhagic infl.
Necrotizing infl.
Allergic infl.

50. Non-suppurative inflammation
Types: (according to features of exudate)
1- Catarrhal infl.
2- Membranous infl.
3- Fibrinous
4- Serous
5- Serofibrinous infl.
6- Hemorrhagic
7- Necrotizing
8- Allergic

51. Chronic inflammation

52. Chronic inflammation Prolonged duration Active inflammation
Tissue destruction
Attempts of healing

53. Chronic inflammation When???? Persistent infections:
Acute infl. fail to cure
Repeated acute infl.
Start de novo (T.B.)
Prolonged exposure to toxic agents
Autoimmunity

54. Morphology of chronic inflammations
Tissue destruction
Blood vessels
Fluid exudate
Cellular exudate

55. Cells of chronic inflammation
Esinophils
Lymphocytes
Plasma cells
Giant cells
Fibroblasts

56. Microscopic picture of chronic inflammation
EAO
EAO
Perivascular infiltrate

57. Microscopic picture of chronic inflammation (cellular exudate)

58. Chronic inflammation
(granuloma)
Specific
Non-specific

59. Compare between acute & chronic inflammation
Onset
Sudden
Gradual
Duration
Short
Prolonged
Vascular phenomenon
Present
Slight/ absent
Cardinal signs
Cells
PNLs, pus cs, macrophages
Lymphocytes, plasma cs, macrophages, giant cs, fibroblasts
Bl.vessels
Thin, dilated, congested
EAO