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Inflammation ( part 1) l General pathology revision

 
مذكرة باثولوجي , مذكرات باثولوجي عامة

Inflammation ( part 1) l General pathology revision for dental and medical student



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ACUTE INFLAMMATION

PATHOGENESIS   


Local tissue changes:

  • Injurious agents cause necrosis with release of chemical mediators that initiate& promote a series of vascular changes.

Local Vascular changes:

  • 1) Transient V.D.       
  • 2) Permanent V.D      
  • 3) vascular permeability with formation of fluid exudate         
  • 4) Slowing of blood flow with vascular stasis
  • 5) Change of normal blood stream with cellular exudation

Local exudative changes

  • 1) fluid exudate. 
  • 2) Cellular exudate: 

  1.       Rolling & margination.     
  2.       Emigration         
  3.       Chemotaxis.       
  4.       Phagocytosis.

 

 

vascular changes ( vascular phenomena )

DEF:

  • A series of vascular changes that bring the defense forces (Plasma and its protein content and leukocytes) to the site of irritant , and its STAGES is :

1.Changes in diameter of blood vessels  

  •    Transient V.C: of arterioles by direct action of the irritant.
  •    Permanent V.D: of arterioles (firstly), venules & capillaries with opening of collapsed capillary bed →↑  blood flow with redness and hotness of the affected area 

- Mechanism:   

  • Direct action of chemical mediators (histamine).      
  • Local axon reflex.

 

2.Changes in wall of blood vessels

  • Increase vascular permeability of venules & capillaries due to widening of inter-endothelial spaces with leakage of protein-rich fluid (fluid exudate)

- Mechanism: 

  1. Direct injury by the irritant                     
  2. Leukocyte-dependent injury
  3. contraction & swelling of endothelium  
  4. Leaking from regenerating capillaries.

 

 

3.Changes in blood flow

  • Slowing of blood flow with vascular stasis.( May cause capillary thrombosis in cases of sever stasis).

- Mechanism: 

  • 1- Increase capillary permeability escape of plasma  fluid exudates with increased blood viscosity (hem-concentration).
  • 2-Resistance of blood flow by the swollen endothelium.
  • 3-Distribution of blood in a large number of dilated capillaries

 

 

4.Changes in blood cells

  • Normally; heavier leukocytes (neutrophils and macrophages) occupy axial stream followed by platelets and RBCs with free peripheral plasmatic zone.

Rolling:

  • Vascular stasis makes RBCs stick together to form rouleux & become heavier than leukocytes & occupy the axial stream then leukocytes cross the peripheral plasmatic zone.

Margination:

  •  leukocytes stick to the endothelium of the venules forming a layer at first with loose adhesions, then with firm adhesion mediated by groups of adhesion molecules between the endothelium and leukocytes

Emigration:

  • The marginated cells then actively move outside the blood vessel towards the irritant ,first cell emigrate is neutrophils followed by monocytes (active process)

“daipedesis”:

  • Some RBCs may be ejected under the effect of hydrostatic pressure through the defect in blood vessel wall (passive process)


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