Acute inflammatory response

• inflammation


  response to tissue injury, attack and removal of cause of injury and repair damaged tissue

  
• 3 inflammation stages

  1. tissue injury = release of histamine

  2. dilation and increased leakiness of capillary = phagocytes migrate to area

  3. phagocytes consume bacteria and cell debris = platelets exit capillary to seal wounded areas

  
• 3 cardinal signs of inflammation

  1. heat

  2. redness

  3. swelling

  4. pain

  5. loss of function

  
• heat + redness

  - arteriolar dilation

  - increased blood flow to inflamed tissue

  
• swelling

  - leakage of plasma from blood vessels into tissue (plasma extravasation)

  - chronic = cellular accumulation, tissue remodelling, fibrin deposition (scarring)

  
• pain

  - external physical/chemical injury trigger sensory nerve to feel pain/itch

  - endogenous generation of chemical mediators of inflammation

  
• tissue mast cells


  - widely distributed throughout connective tissue and mucosal surfaces

  - synthesise and release 'inflammatory mediators' (e.g. histamine)

  - stimuli = mechanical skin injury, type 1 immediate hypersensitivity via IgE (allergy), chemical (e.g. insect bites)

  
• endothelial cells


  - line blood vessels

  - arterial dilation regulated by nitric oxide released from cells

  - contraction makes venules leaky - increasing permeability
• Chemical mediators of inflammation

  - act on microvasculature and tissues

  - low specificity

  - some exist as plasma precursors

  - synthesised/released when required

  
• histamine


  - pre-formed and released from cells when needed

  - relaxes arteriolar smooth muscles

  - contracts venular endothelium so increased permeability

  - also signals sensory nerve (C fibre) to initiate pain response

  
• eicosanoids


  - oxidation products of fatty acids

  - pro- and anti-inflammatory actions
• prostaglandins


  - causes fever to protect against infection and increases metabolism

  - dangerous if prolonged or severe due to enzyme denaturation

  - regulated by production and action of PGE2 in hypothalamus
• leukotrienes


  - oedema = LTC4+LTD4 stimulate increased vascular permeability

  - chemotaxis = LTB4 potent chemotactic agent for inflammatory cells
• why is inflammation beneficial?

  - increases supply of cells and chemical mediators to inflammation site

  - tells body to rest