Inflammation - IntroductionOn inury, the cells either undergo adaptation or necrosis depending upon its severity. At thesame time, the whole tissue will mount a response and is known as inflammation.INFLAMMATION - DEFINITION Inflammation is a reaction of a living vascularised tissue to an injury. e.g., a boil, an acute appendicitis. Inflammation serves to destroy, dilute or wall of injurious agents. It closely intertwined with the process of repair. i.e., Regeneration / ScarringINFLAMMATION - TYPESThe inflammation is broadly divided in to two types.ACUTE INFLAMMATION is of short duration is stereotypic is characterised by oedema & migration of neutrophilsCHRONIC INFLAMMATION Long duration less uniformACUTE INFLAMMATIONCAUSESAcute inflammation can be caused by many agents which include...Physical: Trauma, Heat, cold, Radiation etc.Chemical : Toxins, acid etc.Biological : Bacteria, Virus, Parasite etc
Immunological: Antibody mediated , Cell mediatedNecrotic tissue : Necrotic tissue [as in myocardial infarction]LOCAL SIGNS OF INFLAMMATIONAt the site of injury, the following CHARACTERISTIC signs develop.CARDINAL SIGNS Rubor: Red Calor: Heat Tumour: Swelling Dolar : Pain Functiolaesa : loss of function (may or may not present)PATHOGENESISThe pathogenesis of acute inflammation can be studied conveniantly under the followingthree headings.1. Changes in vascular flow & caliber2. Changes in vascular permeability3. Cellular events : Leukocyte exudation & phagocytosis1. CHANGES IN VASCULAR FLOW AND CALIBER- produce hyperaemia Blood flow in normal area
Blood flow in inflammed area2. CHANGES IN VASCULAR PERMEABILITYproduce local oedemaMECHANISM: (of increased permeability of vessel wall)1. Endothelial contraction• occurs in mild injury• begin directly after injury (Imm.transient leakage)• peak within 5 to 10 mts. & phases out within 15 to 30 mts
• mediated by histamine & other chem. mediators• inhibited by antihistamine -leak exclusively from venules.