Inflammation and wound healing Flashcards
Inflammation
non specific protective response of the body to threats. Involves specialized cells, mediators and inflammatory enzymes which work together to destroy or contain foreign bodies
May be acute or chronic
Acute inflammation
occurs over seconds, minutes, hours or days
rapid response and results in increased blood flow to affected area
Chronic inflammation
occurs over long periods
can occur when acute inflammation does not resolve
Five cardinal signs of inflammation
ruber (redness) calor (heat) tumor (swelling or oedema) delor (pain) functio laessa (loss of function)
Acute inflammation involves several constituents of the immune and vascular systems
Infection Physical injury Radiation Chemical exposure Thermal burns Tissue necrosis Foreign antigens Immune responses
Inflammatory response process
vasodilation ( increased blood flow)
increased vascular permeability ( capillaries allow fluid and proteins to leak into the tissue)
migration of blood borne leukocytes (neutrophils/ polymorphs) into the tissue
How the inflammatory response works
Acute inflammation results in increased blood flow to the affected region. The blood capillaries become more permeable and fluid, inflammatory mediators and leukocytes enter the tissue. Vasodilation and vascular permeability are brought about by the action of histamine, serotonin and other chemical mediators. The fluid that leaks out of the blood vessels generally contains proteins and is therefor called exudate. This fluid will eventually return to the circulatory system via the lymphatic system.
Inflammatory mediators
soluble molecules that act locally. Interleukin 1 (IL-1), interleukin 6 (IL-6) and tumor necrosis factor are important inflammatory mediators that induce the acute inflammatory response
How do neutrophils leave the blood vessels and enter the tissue>
Presence of a number of mediators including TNF alpha induce endothelial cells to increase synthesis of surface adhesion molecules called selectins
The selectins then interact with the neutrophil polymorphs causing the neutrophil polymorphs to roll along the vessel wall
The rolling polymorphs express integrins which bind to intracellular adhesion molecules. This binding stimulates the move through the wall of the blood vessel by pseudopodal movement
Once out of the blood vessels the neutrophil polymorphs move following a chemokine (e.g. C5a ) concentration gradient to the area of damage. C5a also activated the neutrophils causing them to increase in size and synthesize additional toxic granules. The neutrophil polymorphs along with macrophages, phagocytose microbes tagged with C3b , an opsonin and kill them
Neutrophil polymorphs are recruited to the tissue via these steps
Migration-polymorphs lie along the inner wall of the blood vessels
Rollin- polymorphs roll along the vessel wall
Adhesion- polymorphs stick to the vessel wall by means of adhesion molecules
Emigration and chemotaxis- polymorphs move from the vessels into the surrounding tissues and from there to the source of the damage, following a chemokine gradient
Activation- polymorphs become enlarged and armed to kill invaders
Phagocytosis- organism is engulfed in phagosome and this is fused with the lysosome
Killing- phagocytized bacteria are killed
Yellow exudate
pus
4 possible outcomes of acute inflammation
complete resolution ( no permanent damage)
scarring
abscess formation accumulation of pus, bacteria contained but not killed ( pimple)
progression to chronic inflammation
Main cells in acute and chronic inflammation
acute- neutrophil polymorphs
chronic- T lymphocytes, B lymphocytes and antigen presenting cells including macrophages
Two main conditions under which chronic inflammation develops
viral infection
autoimmune reactions
Chronic suppurative inflammation
factors that cause acute inflammation don’t resolve in a few days
is a persistent acute inflammation typified by infiltration with neutrophils and formation of pus