Pathology

1. Inflammation Mr:Mahmoud Ibrahim
Osman

2. The response of living vascularized tissues to
injury
1- Acute inflammation
2- Chronic inflammation

3. Acute inflammation
Early response of tissue to injury
Vascular
Non-specific
Short duration

4. COMPONENTS OF ACUTE
INFLAMMATORY RESPONSE
Vascular
1. Transient vasoconstriction of arterioles : It disappears
within 3-5 seconds in mild injuries
2. Active vasodilatation of arterioles-Histamine-mediated
result in (Hyperemia- increased blood in the area)

5. 3-Increased vascular permeability Histamine-mediated ,
result in (Increased fluid & high MW proteins pass
through widened intercellular junctions)

6. - 4. Formation of fluid exudate, from circulation to the interstitial
tissues. Fibrin-rich fluid
- Contains plasma proteins including Ig, C’ and fibrinogen.
- Helps combat the offending agent by diluting it, increase
lymphatic flow and flooding the area with Ig+C’.

7. Mechanisms of inflammation

8. Pneumonia- exudation

9. Cellular response
. Types of cells involved
1st 24 hours- neutrophils
24 48 hours – macrophages, lymphocytes, plasma
cells.
B. Margination of neutrophils
Due to rouleaux formation of red cells and decreases in
plasma.

10. C. Pavementing of neutrophils
Marginated neutrophils adhere to endothelial surface.
D. Emigration of neutrophils
Neutrophils leave blood vessel through intercellular
junction into interstitial tissue (3-10 mins)

11. E. Chemotactic factors
C5a, leukotriene B4, bacterial products
Neutrophils have receptors for these factors
F. Movement of other cells
Macrophages and lymphocytes also mediated by lymphokines

12. Phagocytosis: Involves:
a) Attachment of opsonized particles to the surface of leukocytes.
c) Engulfment by pseudopods encircling the phagocytosed
particles, creating phagosome. Fusion of lysosomal granules
with the phagosome, leading to degranulation

13. c) Killing and degradation bacteria.
Types of bactericidal mechanisms:
1. O2- dependent mechanism O2→superoxide
2. O2- independent mechanisms e.g lysozyme, lactoferrin

16. Components of acute inflammation
Vascular changes Cellular events
 Vasodilation: alterations
in vessel caliber
resulting in increased
blood flow
 Increased vascular
permeability: permit
plasma proteins to leave
the circulation
 Emigration of the leukocytes
from the microcirculation
and accumulation in the
focus of injury
 Principal leukocytes in acute
inflammation are
neutrophils
(polymorphonuclear
leukocytes).

17. Inflammation serves to destroy, dilute or isolate the
injurious agent (microbes, toxins) and eliminate the
necrotic cells and tissues.

18. The 5 cardinal signs of inflammation
Color—heat
Rubor—redness
Tumor—swelling
Dolor—pain
Functio laesa—loss of function

21. Redness/ Heat
Increased rate and volume of blood flow into inflamed
area
Swelling
Accumulation of exudate in the tissues

22. Pain
Accumulation of chemicals (prostaglandins) that
stimulate nerve endings. Increased tissue tension

23. Mediators of acute inflammation
Vasodilatation
Histamine
Prostaglandins
Nitric oxide

24. Increased vascular permeability
Histamine
Complements C3a, C5a
Bradykinin
Leukotrienes C4,D4, E4
Platelet aggregating factor

25. Chemotaxis/ leucocyte activation
Complement C5a
Leucotriene B4
Bacterial products
Cytokines (IL-8)

26. Fever
Interleukins IL-1, IL-6
Tumour necrosis factor (TNF)
prostaglandins

27. Pain
Prostaglandins
Bradykinin

28. Tissue damage
Lysosomal enzymes (neutrophil, macrophages)
Oxygen metabolites
Nitric oxide

29. Edema
Excess of fluid in the interstitial space.
Either exudates or transudate.

30. Exudates
Inflammatory extravascular fluid with high protein content, cellular
debris, SG 1.012
Transudate
Fluid with low protein content. SG< 1.012

31. Pus
Inflammatory exudate rich in neutrophils and debris

32. Types of inflammatory exudate
Serous ; Fluid exudation. Burns
Fibrinous ; Excess fibrin formation. Bacterial infections.
Membranous / pseudo-membranous . Necrotic exudates
adherent to mucosal surface Diphtheria, antibiotic-assoc. colitis

33. Hemorrhagic ;Marked necrosis and hemorrhage. Virulent organisms
Catarrhal ; Excess mucus, common cold
Suppurative ;Marked neutrophils response with pus.
Pyogenic infections
Allergic :Marked edema. urticaria

34. Cellulitis
Spreading inflammation with tissue necrosis

35. Outcome / Sequelae of acute inflammation
Resolution : Return to normal structure and function
Healing by fibrosis/ later fibrous scar
Suppuration / abscess
Chronic inflammation :Persistence of acute inflammation
converts response to a chronic type

36. Effects of acute inflammation
Beneficial effects
1. Dilution of toxin
2. Entry of antibodies
3. Transport of drugs
4. Fibrin formation
5. Delivery of nutrients & oxygen
6. Stimulation of immune response

37. Harmful effects
1. Enzyme digestion of normal tissues
2. Swelling- causing (respiratory) obstruction and raised
(intracranial) pressure
3. Inappropriate inflammatory response eg. Type 1
hypersensitivity reaction

38. Acute inflammation
 rapid in onset (seconds
or minutes)
 relatively short duration,
lasting for minutes,
several hours, or a few
days
 its main characteristics:
 the exudation of fluid and
plasma proteins (edema)
 the emigration of
leukocytes, predominantly
neutrophils.
 is of longer duration
 associated histologically
with the presence of
lymphocytes and
macrophages, the
proliferation of blood
vessels, fibrosis, and tissue
necrosis.
 Less uniform.
Chronic inflammation