The inflammatory
response is both normal and necessary.
A non specific response.
Inflammation
literally means, "to set afire".
Suffix
"itis" is used to describe an inflammatory response.
Inflammation
is the first stage in the healing process.
Loss of function
Mechanical trauma
Chemical agents
Thermal injuries
Immunological
reactions
Infection
Radiation
Mechanical trauma
Cuts, abrasions,
crush injuries, friction, pressure
Chemical agents
Acids, alkalis, some
organic compounds, alcoholic gastritis or hepatitis, biliary peritonitis,
pancreatitis,
Thermal injuries
Heat, cold
Immunological reactions
Rheumatoid arthritis
Asthma
Allergic reactions
Radiation
Ultraviolet light in sunshine
Infection
Conjunctivitis
Meningitis
Encephalitis
Gastritis
Cholecystitis
Conjunctivitis
Cystitis
Pyelonephritis
Colitis
Tonsillitis
Appendicitis
Peritonitis
Pneumonitis, pneumonia
Urethritis
Dermatitis - eczema
Wound infection
Abscess
Vasodilation
Increased capillary permeability
Production of inflammatory exudate
Clotting of fluid in the extracellular spaces
Walling off, blocking local tissue spaces and lymphatics
Migration of granulocytes then monocytes, lymphocytes, plasma cells
Phagocytosis, antibody production, cytokines, growth factors.
There are numerous substances that act as inflammatory mediators including histamine and prostaglandins.
Histamine
Tissue insult
Mast cell degranulation
Histamine
Vasodilation
Nociceptors sensitization
Antihistamines block histamine receptors by competitive blockage of tissue bound histamine receptors
Prostaglandins
Cell membrane phospholipid released into tissues
Phospholipase A
(Corticosteroids inhibit the activity of this enzyme)
Arachidonic acid
Cyclo-oxygenase COX (NSAIDs and aspirin inhibit COX activity)
Prostaglandins
The
purpose of inflammation
Hyperaemia will
increase the blood supply so increase glucose and oxygen delivery.
Increases in the
supply of amino acids, vitamins and minerals.
Fibrinogen enters the
tissues to compartmentalise infected areas.
Leucocytes migrate
into tissue spaces to phagocytose.
Leucocytes also
release chemical mediators.
Pain and muscle
splinting promote immobilisation.
Therefore
inflammation is essential for healing.
1. Tissue macrophages
2. Neutrophil dipedesis and chemotaxis
3. Neutrophilia within a few hours from 4 – 5 000 up to 25 000 as a result of inflammatory mediators entering the blood
4. Monocyte migration followed by cell enlargement into macrophages
5. After 3 – 4 days monocyte and granulocyte production in bone marrow is increased (production rates may be 20 – 50 times normal)
Often collects in a hollowed out area
Dead granulocytes and macrophages
Dead and phagocytosed tissue cells
Dead and living bacteria
Tissue fluid
If not evacuated pus will autolyze and gradually be absorbed into surrounding tissue
Resolution
Scaring
Chronic inflammation / abscess formation
Spread
Death
Inflammation which lasts for more than 2 weeks
Triggered by the release of inflammatory mediators into the blood.
Collectively these can be called the acute phase reactions.
Fever, pyrogens
Acute phase proteins – increased production of clotting proteins, C-reactive protein and complement.
Leucocytosis.
Bacterial infections – neutrophilia.
Viral infections – lymphocytosis.
Allergies or parasitic infection – eosinophilia.
Trauma or stress increases ADH, ACTH, adrenaline and growth hormone.
Metabolic changes lead to malaise, weakness, loss of appetite.
When an area is injured and painful,
local muscles are stimulated to contract and protect the injury. For example if
you sprain an ankle the lower leg muscles will tighten to `splint` the injured
area. This reaction is referred to as muscle `guarding`.
Maggots introduced onto a wound also
preferentially eat dead (necrotic) tissue. In this sense there debridement role
is similar to phagocytes. (Debride means to remove foreign or dead material
from a wound). This is the basis of the revival of the ancient treatment of
larval therapy.
Poor healing is observed in patients
taking corticosteroid drugs which inhibit the inflammatory response.