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Path - Acute inflamm (i) (Acute (5 classic local signs (macroscopic…

- - - - due to endothelial injury
      - cell contraction + junction retraction
      - exudation of protein rich fluid with neutrophils (exudate)
        
        blood now has increased RBC conc + viscosity, leading to stasis (disrupts laminar flow)
  - - - Margination
        
        neutrophils normally travel in centre of vessel with RBCs while plasma flows in periphery (laminar flow) + other WBCs, but instead now move to periphery due to stasis to be in contact with endothelium
      - Endothelial activation
        
        mediator release, selectins move to surface
      - Rolling adhesion
        
        carbs on neutrophils transient bind with selectins
      - tight binding
        
        integrins on neutrophils firmly adhere to ICAM1/VCAM1 on endothelial cells
        
        aka pavementing
      - transmigration/diapedesis
        
        neutrophils squeeze through gaps in endothelial cells
        
        via PECAM1/CD31
      - chemotaxis
        
        neutrophils move towards site of injury due to secretion of chemoattractants (chemokine IL8)
        
        recognise microbes + dead tissues via TLRs
        
        upreg of NK kappa beta
- - - - high @ arteriolar end so fluid out
      - low @ venue end so fluid in