The inflammatory response is both normal and necessary.
A non specific local response to a recent or ongoing insult.
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
Dermatitis - eczema
Cuts, abrasions, crush injuries, friction, pressure
Acids, alkalis, some organic compounds, alcoholic gastritis or hepatitis, biliary peritonitis, pancreatitis.
Ultraviolet light in sunshine
Increased capillary permeability
Production of protein rich 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; they may be derived from plasma or cells. Kinins (e.g. bradykinin), clotting factors and complement are inflammatory mediators derived from plasma.
Mast cell degranulation
Histamine (and some bradykinin)
Antihistamines block histamine receptors by competitive blockage of tissue bound histamine receptors.
Prostaglandins and Leukotrienes
Cell membrane phospholipid released into tissues
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.
Exudate will dilute toxins.
Pain and muscle splinting promote immobilisation.
Fibrinogen enters the tissues to compartmentalise infected areas, blocks lymphatics.
Leucocytes migrate into tissue spaces to phagocytose.
Leucocytes also release chemical mediators.
Therefore inflammation is essential for healing.
1. Tissue macrophages, activated by tissue damage to release cytokines which in turn attract other inflammatory cells.
2. Neutrophil diapedesis and chemotaxis (many found in inflammed tissue 90 minutes after injury, peaking at 24 – 48).
3. Neutrophilia within a few hours from 4 – 5 000 up to 20 000 as a result of inflammatory mediators entering the blood. Neutrophils are released from the bone marrow.
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).
(Increased production of neutrophils and monocytes is stimulated by cytokines from activated monocytes in the inflamed tissues).
Often collects in a hollowed out area.
Dead granulocytes and macrophages.
Dead and phagocytosed tissue cells.
Dead and living bacteria.
If not evacuated pus will autolyze and gradually be absorbed into surrounding tissue.
Suppurate – to produce pus
Purulent – contains lots of pus
Empyema – pus filling a cavity
Chronic inflammation / abscess formation
Inflammation which lasts for more than 2 weeks.
Causes include parasites, bacteria, viruses, ongoing trauma, cancer, autoimmunity.
Many mononuclear cells, (monocytes, lymphocytes, plasma cells) present.
Do not mask clinical features
Establish priorities, e.g. airway swelling
Keep warm (usually)
Triggered by the release of inflammatory mediators and cytokines into the blood.
Collectively these can be called the acute phase reactions.
Skeletal muscle catabolism.
Lethargy (cytokines affecting CNS).
Acute phase proteins – increased production of clotting proteins, C-reactive protein and complement.
Trauma or stress increases ADH, ACTH, adrenaline and growth hormone.
Metabolic changes lead to malaise, weakness, loss of appetite.
Bacterial infections – neutrophilia.
Viral infections – lymphocytosis.
Allergies or parasitic infection – eosinophilia.