1. INFLAMMATION By Dr: Gehan Mohamed Dr. Abdelaty Shawky

2. Intended Learning outcomes (ILOs):
Understanding the definition of Inflammation.
Listing the classification of inflammation.
Identifying the pathogenesis of Acute Inflammation.
Recognizing the difference between acute and chronic inflammation regarding the onset, causes and microscopic picture.
Outlining the mechanism of formation and function of the inflammatory fluid exudate.

3. Listing the types of acute inflammation.
Understanding the pathological features of pyogenic abscess and cellulitis.
Understanding the pathological features of acute non-suppurative inflammation.
Recognizing the definition, types and pathological features of chronic inflammation.
Be aware of the definition and types of granuloma.

4. Inflammation
* Definition: Local vascular, lymphatic and cellular reactions of living tissue against an irritant.
*Inflammation is a protective mechanism with the purpose of:
To defend against and to eliminate the injurious agent responsible for injury.
Removal of the consequences of injury (necrotic cells).
To start repair of injured tissue.

5. * Nomenclature of inflammation:
Inflammation is designated by adding the suffix “itis” to the English, Latin or Greek name of the organ affected :
Examples:
Appendix  appendicitis
Pancreas  pancreatitis
Meninges  meningitis
Pericardium  pericarditis
Liver  hepatitis
Joints  Arthritis

6. * 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. (d) Immunological: e.g. allergic inflammation.

7. TYPES OF INFLAMMATION (1) Acute Inflammation:
Characterized by sudden onset and short duration (days to weeks).
(2): chronic inflammation:
Characterized by gradual onset and long duration (months to years).
(3): subacute inflammation:
Between the acute and the chronic types.

8. Acute Inflammation

9. * Pathogenesis of acute Inflammation: The acute inflammatory reaction consists of: I. Local tissue damage. II. Local vascular reactions. III. Chemical mediators .

10. I. Local tissue damage:
Occurs at the centre of the inflamed area with the maximum concentration of the irritant resulting in. Local death of tissue (necrosis).
This local damage of cells together with inflammatory stimulus trigger the release and activation of chemical substances called chemical mediators as histamine, serotonin and prostaglandins.
These chemical mediators play an important role in promoting the vascular and cellular changes in the inflamed area.

11. II. Local vascular reactions

12. 1.Transient vasoconstriction of the small arterioles:
- Occur in this sequence:
1.Transient vasoconstriction of the small arterioles:
Caused by the direct effect of the irritant on the vascular wall.
Vasoconstriction is a protective mechanism and lasts for seconds to minutes only.

13. 2. Vasodilatation of the arterioles, venules and capillaries:
Caused by:
a. Direct action of histamine on the vascular wall. b. Local axon reflex.
The dilatation of the arterioles and capillaries will increase the blood flow & is called hyperaemia. The inflamed area becomes red and hot.

14. 3. Slowing of the Blood Stream (Stasis):
Caused by:
a. Increased viscosity of the blood due to formation inflammatory fluid exudates. This is the main cause of stasis.
b. Histamine causes swelling of the vascular endothelium which become sticky and offer mechanical resistance to the blood.

15. 4. Formation of the Inflammatory Exudates: The intravascular contents (plasma and cells) escape into the interstitial tissue spaces forming the inflammatory exudates which consists of a fluid component and a cellular component (leucocytes). 5. Dilatation of lymphatic vessels: to accelerate the lymph flow and drains the fluid exudates.

16. Exudation
The escape of intravascular plasma fluid & leucocytes to the interstitial tissue of the inflamed area. Occurs when blood vessels become leaky.
Inflammatory fluid exudate: an inflammatory extravascular fluid with a high protein concentration, cells/cell debris & an SG (specific gravity) > 1020.
Inflammatory cellular exudate: passage of leucocytes to the extravascular interstitial to attack the irritant.

18. Exudate : microscopy
Neutrophils
Exudate rich in fibrin

19. Note: Transudate:
Is an extravascular fluid with a low protein content, few or no cells & SG < 1012.
Results due to imbalance in hydrostatic pressure.
Occurs when there’s organ failure as heart failure leading to systemic congestion and formation of transudate.
Q. List the differences between exudate and transudate.

20. A. The Inflammatory Fluid Exudate
* Mechanism of formation:
1. Increased capillary permeability caused by histamine (the main cause).
2. Increased capillary hydrostatic pressure due to dilatation of the arterioles and increased blood flow.
3. Increased osmotic pressure of the interstitial tissue fluid as the large protein molecules split into smaller ones in the process of tissue necrosis. This acts as a suction force from the capillaries.

21. * Characters: - High fibrinogen content (turbid & clots on standing).
- High protein content, 4-8 gm% (the normal interstitial tissue fluid contains 1 gm% protein).
- High fibrinogen content (turbid & clots on standing).
- High specific gravity (above 1018).
- High cellular content (polymorphs & macrophages)

22. * Functions: 1. It dilutes toxins, chemicals and poisons, so minimizes their effects. 2. Brings antibodies from the blood to the site of inflammation. 3. Supplies nutrition for the cells and carries away waste products. 4. Fibrinogen forms a fibrin network, which acts as a mechanical barrier to the spread of infection and as a bridge for leucocytes to reach the irritant.

23. Thanks