Inflammation -2

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Shared by: Amit Kashyap
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Transudate Vs Exudate TRANSUDATE  EXUDATE  is protein-poor ultra filtrate of plasma increased hydrostatic pressure. protein-rich fluid which has leaked out of inflamed vessels. Occurs due to inflammation It contains neutrophils and necrotic debris (pus). Specific gravity of > 1.020     Specific gravity 1.010  Chemotaxis CHEMOTAXIS The movement of leukocytes towards the site of injury along a chemical gradient of chemoattractants Exogenous and endogenous stimuli can act as chemoattractants Exogenous: bacterial product Endogenous: anaphylatoxins (C5a), leukotrienes (LTB4), Cytokines (e.g IL-8)    Chemotactic agents bind to the surface leucocytes Calcium mobilization and assembly of actin filaments Leukocytes extend pseudopods and migrate towards the stimuli Phagocytosis or Killing Derived from the Greek words “Eat , cell”. - Cellular process of eating  Phagocytosis is carried out by white blood cells: Neutrophils, macrophages, and occasionally eosinophils. Phagocytosis Responsible for elimination of injurious agents Involves 3 distinct steps : Recognition & attachment of the particle to the leucocyte Its engulfment Killing & degradation of the ingested material  1. 2. 3. 1. Recognition & attachment Recognition and Binding  How do the leucocytes recognise the injurious agent ? by a process known as OPSONISATION Complement components (C3b) IgG bind to microbial surface and this coating is required for recognition of the microbe or foreign particle Engulfment   Extension of plasma membrane to form psuedopods around the particle and engulfment to form a sac called phagosome Inside the cell, phagosome fuses with lysosome to form phagolysosome Killing   Oxygen dependent Oxygen independent Oxygen dependent killing H2O2 - MPO – Halide system 2 the most efficient O is NADPH OXIDASE MPO bactericidal system in O2 CL H2O2 OHHOCL neutrophils. H2O2 –MPO –Halide system Reactive oxygen species    Hydrogen peroxide (H2O2) MPO (azurophilic granules) converts hydrogen peroxide to HOCl- (in presence of Cl-) Killing of microbes by halogenation(HOCL), or lipid/protein peroxidation Oxygen independent killing  Other antimicrobials in leukocyte granules Bactericidal permeability increasing protein (BPI) Lysozyme Lactoferrin: iron binding protein present in the neutrophil Defensins (punch holes in membranes) Defects in leucocyte function Genetic Acquired Leucocyte Adhesion Deficiency - (LAD)  LAD 1 : Defective integrins Lead to recurrent bacterial infections,  LAD 2 : Defective selectins Lead to recurrent infections – Milder form Defect in phagolysosome function Chediak- Higashi Syndrome Defective degranulation Delayed microbial killing Giant neutrophil granules Defective microbicidal killing  Myeloperoxidase deficiency : Absent MPO-H2O2 system Chronic Granulomatous Disease: Inherited defect in genes coding NADPH oxidase  defective formation of reactive O2 species.  Outcome of acute inflammation RESOLUTION INJURY ACUTE INFLAMMATION CHRONIC INFLAMMATION FIBROSIS / SCAR Outcome of acute inflammation  Complete resolution  due to elimination of the offending agent and regeneration of injured tissue with normal function  Healing by connective tissue replacement (fibrosis/scar formation) Occurs after large tissue destruction,  tissue without regeneration capabilities   Progression to chronic inflammation Resolution Staphylococcal infection Patterns of acute inflammation Serous inflammation Purulent inflammation Fibrinous inflammation ulcers Patterns of acute inflammation   SEROUS Watery, protein-poor effusion (e.g., blister) FIBRINOUS  Fibrin accumulation Presence of pus (pyogenic staphylococcu spp.) Necrotic and eroded epithelial surface  SUPPURATIVE/PURULENT   ULCERATION 

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