Lecture notes
Inflammation and Wound Healing
- Institution
- Cardiff University (CF)
Concise lecture notes covering the physiology of inflammation and wound healing. Perfect to help consolidate knowledge for pre-clinical students.
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Inflammation and Wound Healing (Lectures Combined)+ BruisingInflammation:
Inflammation is the response of the body to trauma/cell injury/cell death. It happens because the
body is trying to limit the damage that is happening to it and helping to repair, and regenerate
whenever exposed to stress and noxious stimuli. Stress to the body isn’t just emotional stress but
also physical e.g. heat, abrasions, injury, chemicals and drugs. Hence, you treat the signs and
symptoms of inflammation. The body responds to stress in 4 limited ways: hyperplasia (increase in
number of cells e.g. bladder), hypertrophy (increase in size of cell e.g. left ventricle), atrophy
(decrease in size of cell e.g. decrease in size of brain ventricles) and metaplasia (one cell type
replaced by another cell type e.g. oesophagus- exposure to acid: squamous → columnar epithelium
to release basic mucous). So this is how cells try to adapt to stress, if they can’t adapt or they
undergo very serious injury which causes cell injury/death = inflammation.
Cell death via necrosis or apoptosis so
cell death/injury is indicative of
inflammation. However, cells
normally do die e.g. skin, mucosa= no
inflammation.
Necrosis- lysis/cotton candy like, Apoptosis- cell broken up into
this necrotic material is droplets which are eaten up by
important component of pus. phagocytes
Cell Injury causing agents:
• Hypoxia e.g. brain cannot be deprived of oxygen for longer than 4 minutes.
• Ischaemia (lack of blood supply) – less oxygen delivery and waste taken away.
• Physical agents e.g. heat
• Chemical agents and drugs
Infectious agents also cause cell injury (externally) as well as immunological reactions, genetic
derangements (e.g. sickle cell anaemia – damage capillaries) and nutritional imbalances. So all these
potential cell injury causers induce inflammation.
, ➢ The stimuli that cause cell injury also induce inflammation in vascularised tissue, so
not in lens tissue.
The aim of inflammation is to neutralise the offending agent and to start the process of repair. So,
getting rid of the harmful stimulus and then repairing (hence involved in wound healing process, its
all occurring simultaneously).
Cardinal Signs of Inflammation:
• Rubor- redness (due to vasodilation so increased blood supply there)
• Tumor- swelling (due to leakage from vessels into tissue)
• Dolor- pain (nerve endings stimulated, reduced threshold- sensitised)
• Calor- heat (increased blood flow, TRPV1 channels stimulated, increased metabolic activity
of neutrophils)
• Loss of Function- due to pain and swelling etc
➢ The major components of inflammation are vascular changes and cellular changes.
Neutrophil is the cell of acute inflammation and the cell of chronic inflammation is the macrophage.
So, whatever the neutrophil is doing in acute inflammation, the macrophage does in chronic- due to
short life span of neutrophil (after which macrophages take over). Be able to identify cells of blood.
Monocyte in circulation but known as macrophage when it enters the tissue.
➢ The major components of inflammation are vascular changes and cellular changes.
Vascular changes: aim is to get neutrophil from blood into the tissues where inflammation is
happening and get rid of what’s causing it and start process of repair.
This occurs when inflammation is initiated, the first
step in inflammation is vasodilation due to histamine
(mast cells, endothelial cells and wbc), thrombin and
NO (endothelial cells, wbc) which leads to increased
permeability so allowing cells and fluid to move in and
out between blood and tissue via endothelial cell
retraction. They also cause stasis (blood flow slowing
down) which causes cells to move to the edge of the
blood vessels so neutrophil reach edges of blood vessel
in order to ender the tissue. When the injury is more
severe e.g. burn which damages blood vessels, so the
endothelial cells are damaged, this causes the gaps in
vessel walls to last longer (compared to just
vasodilation – short lasting inflammation as retracted
cells return to original shape) so more fluid and cells
leave causing more severe and long-lasting
inflammation. So, allows injuries to be distinguished
based on inflammation length and cause. Macrophages
occurring in tissues also contribute slightly by releasing
TNF-a as well as CXCL-8 to allow adhesion of neutrophil
and make endothelium leaky.
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