prac 2

• 5 steps of inflammatory response

  recognition of injurious agent, recruitment of cellular mediators, removal of the agent, regulation of immune response, resolution or repair
• vasodilation

  histamines and prostaglandins
• increased vascular permeability

  histamine, serotonin, c3a, c5a, and leukotrienes
• chemotaxis and leukocyte recruitment

  TNF, Il-1, chemokines, c3a, c5a, and leukotrienes
• fever

  il-1, TNF, prostaglandins
• pain


  prostaglandins and bradykinin
• tissue damage

  lysosomal enzymes of leukocytes, reactive oxygen species
• resolution happens when:

  injury is limited, minimal tissue destruction, and/or damaged parenchymal cells can regenerate
• resolution involves

  removal of cellular debris by macrophages, resorption of oedema fluid, and regeneration of damaged tissue
• healing by connective tissue replacement happens when:

  there is substantial tissue destruction, tissues are incapable of regeneration, and/or excess fibrin exudate present
• healing by connective tissue replacement involves

  CT growing into the area of damage, converting it into a mass of fibrous tissue
• serous inflammation

  exudation of cell poor fluid (few leukocytes) eg, skin blisters
• fibrinous inflammation

  large vascular leaks (allowing larger molecules such asfibrinogen to leak out)
• Purulent Inflammation

  cell rich (neutrophil) and oedema fluid
• giant cells

  come from TNF-a and IFN-y during immune response, leading macrophages to form giant cells
• ulcer

  localised defect in the mucosa or epidermis, extending through the full thickness
• immune cells in chronic inflammation

  lymphocytes, plasma cells, macrophages
• granulation tissue components

  new blood vessels, proliferating fibroblasts, interspersed leukocytes
• abnormalities of tissue repair

  hypertrophic scars, exuberant granulation tissue, wound dihiscence, ulceration, wound contractures, keloids