21 - Inflammation and Healing II - Outcomes, Mediators and Healing Flashcards
Mediators of acute inflammation 1) 2) 3) 4) 5) 6) 7)
1) Vasodilation
2) Increased vascular permeability
3) Endothelial activation
4) Chemotaxis
5) Tissue damage
6) Pain
7) Fever
Mediators of vasodilation in acute inflammation
Histamine, nitric oxide, prostaglandin, etc.
Mediators of increased vascular permeability in acute inflammation
Histamine, serotonin, bradykinins, leukotrienes
Mediators of endothelial activation in acute inflammation
TNFa, IL-1
Mediators of chemotaxis in acute inflammation
Complement fragments, bacterial fragments, IL-8, Leukotriene B4
Mediators of pain in acute inflammation
Prostaglandins, bradykinin
Mediators of fever in acute inflammation
IL-1, IL-6, TNFa, prostaglandins
What is cyclooxygenase, and by extension prostaglandins, derived from?
Arachidonic acid
Prostacyclin
Arachadonic acid derivative.
Produced by normal epithelial cells.
Vasodilator, inhibits platelet aggregation
Outcomes of acute inflammation 1) 2) 3) 4)
1) Eradicate cause
2) Deal with exudate
3) Replace damaged cells (replenish or replace with scar tissue)
OR
4) Inflammation continues
How is exudate from inflammation dealt with?
Macrophages take up debris, fluid drains into lymphatic system
Three divisions of cells, based on replicative ability
1) Labile (constantly in cell cycle)
2) Stable or facultative dividers (can enter cell cycle if prompted)
3) Permanent (terminally differentiated)
Location of stem cells in GIT
Crypts
Healing involves migration and proliferation of which cells?
• Epithelium in epithelial tissues
• Fibroblasts, myofibroblasts and endothelial
cells which form scar tissue, generally via the
formation of granulation tissue
Granulation tissue
Occurs in healing. Generates scar tissue