Acute Inflammation Lecture One 2015 PDF

Acute Inflammation  Inflammation :Definition The local response of living tissues to injury. due to any agent So it is body defense reaction in order to : eliminate or limit the spread of injurious agents as well as to remove the.consequent necrosed cells and tissues : Inflammation in...

Acute Inflammation  Inflammation :Definition The local response of living tissues to injury. due to any agent So it is body defense reaction in order to : eliminate or limit the spread of injurious agents as well as to remove the.consequent necrosed cells and tissues : Inflammation involves 2 basic processes.inflammatory response -1.healing process -2  Inflammation is complex host response for survival and complex process involve host cells ①. blood Vesseles ②. proteins and other mediates ③. the inflammation divided in to acute inflammation and chronic inflammation the suffix itis mean inflammation example appendix - appendicitis thyroid → thyroditis but Some exception lung → pneumonia  Signs of Acute Inflammation redness(rubor) -1 swelling (tumor) -2 heat (calor) -3 pain(dolor) -4 And last thing the fifth sign loss of function - 5  Acute inflammation short duration.(minutes,hours,few days)-1.represent the early body reaction-2.usually followed by repair-3  Acute inflammation changes :vascular events -1 Accumulation of fluid exudate and.neutrophils in tissues controlled by variety of chemical -2.mediators derived from plasma or cells protective but can lead to local-3.complications or systemic effects  although the inflammation is defence Mechanism but it lead to harmfual effect due to Sever injury ① persistent of infection resist killing ② to word self antigen③  Causes of acute inflammation Microbial Infections – ex: Pyogenic -1.organisms.Hypersensitivity reactions (acute phase) -2.Physical agents -3.Chemicals -4.Tissue necrosis-5  all inflammatory response controls by mediator which is most activited locally at the site of inflammation and have short half life and rapidly decay  Acute inflammation the steps of inflammation is recognition of injurious agent ① recruitment of leukocytes ② removal of agent③ reglation control of response④ resolution ( repair process )⑤  Acute inflammation The vascular changes include Change in calibat _vasodilation_ increase.permeability _ edema formation The cellular changes include Margination and rolling _ emigration _ transmigration and chemotaxis_ activation ,and phagocytosis  Vascular events.haemodynamic changes -1.vascular permeability changes -2  Changes in vascular flow and calibre Transient vasoconstriction of arterioles (few-1.secs) Vasodilatation of arterioles and then capillaries -2 ,so lead to increase in blood flow (heat and.redness) Increased permeability of blood vessels--->-3 exudation of protein – rich fluid into tissues slowing of circulation increase-1 fluid flow out of vessel Increase colloid osmotic pressure of -2 interstitium ---> increase fluid flow out of.vessel  Fluid exudation Acute inflammation arteriolar dilatation leads to increase in-.hydrostatic pressure increased permeability of vessel walls leads-.to loss of protein into interstitium.Net flow of fluid out of vessel  Exudate vs Transudate :Exudate -1.A- Fluid loss in inflammation.B-high protein content C-specific gravity above 1.02 :Transudate -2 A-Fluid loss due to hydrostatic pressure imbalance only (eg. venous outflow (Obstruction.B-low protein content.C-specific gravity less than 1.012  Oedema ,Oedema = excess of fluid in interstitium.can be transudate or exudate Oedema leads to increased lymphatic.drainage Pus = a purulent exudate, rich in.neutrophils and cell debris  Migration of neutrophils Stasis causes neutrophils to line up at the-1 edge of blood vessels along the.endothelium = MARGINATION Neutrophils then roll along endothelium,-2.sticking to it intermittently = ROLLING.Then stick more avidly = ADHESION -3 Followed by EMIGRATION of neutrophils -4.through blood vessel wall  Neutrophil chemotaxis and phagocytosis Neutrophils migrateto site of injury under -1. influence of chemotacticagents chemotaxis = migration along a chemical).(gradient.Neutrophils phagocytosemicroorganisms -2 Activated neutrophils may release toxic -3 metabolites and enzymes causing damage.to the host tissue Hallmark of acute inflammation A -EXUDATE (of FLUID). B- INFILTRATE (of CELLS).  How do these changes combat ?injury Exudation of fluid-1. Delivers plasma proteins to area of injury immunoglobulins inflammatory mediators fibrinogen Dilutes toxins Increases lymphatic drainage Delivers micro-organisms to phagocytes and antigens to immune system 2.Infiltration of Cells: Removes pathogenic organisms, necrotic debris. 3. Vasodilatation: Increases delivery, increases temperature. 4. Pain and loss of function: Enforces rest, reduces chance of further traumatic damage.