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
Components of granulation tissue 1) 2) 3) 4) 5)
1) Macrophages and lymphocytes
2) New blood vessels
3) Migrating fibroblasts
4) Deposited ECM
5) Granulation tissue initially cellular and vascularised, later becomes mostly fibrous tissue (collagen = scar tissue)
Vascularisation in granulation tissue 1) 2) 3) 4) 5)
1) Degradation of basement membrane by matrix metalloproteinases (MMPs) and loss of
cell to cell contact between endothelial cells
2) Migration and proliferation of endothelial cells toward angiogenic stimulus
3) Maturation of cells, recruitment of pericytes and smooth muscle cells
4) New vessels are leaky
5) VEGF secreted by various mesenchymal cells important
Name for healing of clean wounds with closely-opposed edges
Healing by primary intention
Part of damaged tissue that can regrow
Epidermis can grow over the top of scar tissue
Juxtacrine
Signalling between cells that are next to each other.
Often occurs when transmembrane proteins are between communicating cells
Growth factors in repair
1)
2)
3)
1) Released by many cell types in inflammation (EG: immune cells, epithelial)
2) Activate c-MYC, c-JUN, p53 in target cells, often through tyrosine-kinase activity
3) Lead to proliferation of epithelium, endothelium, fibroblasts
Example of a signal transduction pathway involved in healing that isn’t linked to a tyrosine-kinase receptor
JAK/STAT
How does an abscess form?
Marked neutrophilic response leads to tissue destruction
Why are abscesses hard to treat?
Bacteria are in middle of puss, neutrophils and antibiotics can’t reach this, as it isn’t vascularised.
If chronic, a fibrous capsule can form around it.
Two types of healing possible
Resolution - Complete restoration of normal tissue, without scarring.
Healing by repair - Scar formation.
Example of healing by resolution
Lobar pneumonia, if antibiotics are given quickly, as only epithelial cells are damaged, and these can regenerate
Name for a wound coming open
Dehiscence
