INFLAMMATION
Acute inflammationChronic inflammation
Repair
Resolution
Abscess
Injury
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“Inflame” – to set fire.Inflammation is “A dynamic response of vascularised tissue to injury.”It is a protective response.It serves to bring defense & healing mechanisms to the site of injury.
What is Inflammation?
A reaction of a living tissue & its micro-circulation to a pathogenic insult. A defense mechanism for survival .Reaction of tissues to injury, characterized clinically by: heat, swelling, redness, pain, and loss of function. Pathologically by : vasoconstriction followed by vasodilatation, stasis, hyperemia, accumulation of leukocytes, exudation of fluid, and deposition of fibrin.
How Does It Occur?
The vascular & cellular responses of inflammation are mediated by chemical factors (derived from blood plasma or some cells) & triggered by inflammatory stimulus. Tissue injury or death ---> Release mediators
Etiologies
Microbial infections: bacterial, viral, fungal, etc. Physical agents: burns, trauma--like cuts, radiation Chemicals: drugs, toxins, or caustic substances like battery acid. Immunologic reactions: rheumatoid arthritis.Cardinal Signs of Inflammation
Redness : Hyperaemia. Warm : Hyperaemia. Pain : Nerve, Chemical mediators. Swelling : Exudation Loss of Function: PainTime course Acute inflammation: Less than 48 hours Chronic inflammation: Greater than 48 hours (weeks, months, years) Cell type Acute inflammation: Neutrophils Chronic inflammation: Mononuclear cells (Macrophages, Lymphocytes, Plasma cells).
Pathogenesis: Three main processes occur at the site of inflammation, due to the release of chemical mediators : Increased blood flow (redness and warmth). Increased vascular permeability (swelling, pain & loss of function). Leukocytic Infiltration.
Mechanism of Inflammation
Vaso dilatation Exudation - Edema Emigration of cells ChemotaxisExudate: A filtrate of blood plasma mixed with inflammatory cells and cellular debris. permeability of endothelium is usually altered high protein content.
Pus: A purulent exudate: an inflammatory exudate rich in leukocytes (mostly neutrophils) and parenchymal cell debris.
Leukocyte exudation
Divided into 4 steps Margination, rolling, and adhesion to endothelium Diapedesis (trans-migration across the endothelium) Migration toward a chemotactic stimuli from the source of tissue injury. PhagocytosisPhagocytosis
3 distinct steps Recognition and attachment Engulfment Killing or degradationChemical Mediators:
Chemical substances synthesised or released and mediate the changes in inflammation.Histamine by mast cells - vasodilatation.Prostaglandins – Cause pain & fever.Bradykinin - Causes pain.Morphologic types of acute inflammation
Exudative or catarrhal Inflammation: excess fluid. TB lung.Fibrinous – pneumonia – fibrin Membranous (fibrino-necrotic) inflammationSuppuration/Purulent – Bacterial - neutrophilsSerous – excess clear fluid – Heart, lungAllergic inflammationHaemorrhagic – b.v. damage - anthrax.Necrotising inflammation.
Acute inflammation has one of four outcomes:
Abscess formation Progression to chronic inflammation Resolution--tissue goes back to normal Repair--healing by scarring or fibrosisAbscess formation:
"A localized collection of pus (suppurative inflammation) appearing in an acute or chronic infection, and associated with tissue destruction, and swelling.Site: skin, subcutaneous tissue, internal organs like brain, lung, liver, kidney,…….Pathogenesis: the necrotic tissue is surrounded by pyogenic membrane, which is formed by fibrin and help in localize the infection.