Inflammation PDF

Prof Noha ElKady Professor pathology department Faculty of Medicine Objectives  Define inflammation  Differentiate between acute and chronic inflammation  Recognize the steps of extravasation of inflammatory cells  Recognize the process of chemotaxis and phagocytosis...

Prof Noha ElKady Professor pathology department Faculty of Medicine Objectives  Define inflammation  Differentiate between acute and chronic inflammation  Recognize the steps of extravasation of inflammatory cells  Recognize the process of chemotaxis and phagocytosis  Identify different examples of inflammation  Definition Local vascular and cellular response of living tissue against an injurious agent Aims of inflammation Fighting bacteria Localize infection Removal of damaged tissue Causes of inflammation Types of inflammation 1- Acute 2- Chronic  Cells in acute and chronic inflammation  Neutrophils: phagocytosis, pus cells  Lymphocytes: chronic  Plasma: chronic  Histiocytes: Chronic phagocytosis, monocytes  Eosinophils: allergy, parasitic  Mast cells: allergy (histamine, serotonine)  Giant cells: phagocytosis, histiocytes,  Acute & Chronic Inflammation Features Acute Chronic Onset Fast: minutes to hours Slow; days Cellular infiltrate Neutrophils mainly Monocytes/macrophages & Lymphocytes Tissue injury, fibrosis Usually mild and self Often severe and limited progressive Local & Systemic signs Prominent Less prominent Local signs of Inflammation The main events of inflammation 1- vascular response 2- inflammatory fluid exudate 3- inflammatory cellular exudate 1) Vascular Response  (1)Changes in Vascular Flow and Caliber  Vasodilatation (histamine)  Stasis (+ viscosity, swollen end.,open capillaries) 2) INCREASED PERMEABILITY and formation of fluid exudate  Histamine, Kinine  Endothelial “gaps”  Direct endothelial Injury 2)Inflammatory fluid exudate  Formation:  1-VD, +Permeability  2- + interstitial osmotic  3- -hydrostatic  Function:  Dilute toxin, chemical, poison  Bring antibodies  Supply nutrition for cells remove toxins  Supply fibrinogen ( localization, movement of inflammatory cells and fibroblasts  Composition of Exudate Appearance: Turbid Consistency: Viscous (like pus) Protein content: high 4-8 gm Specific gravity: high above 1018 Cell content: numerous neutrophilis On standing: clots 3) Cellular exudate EXTRAVASATION of neutrophils  MARGINATION (PMN’s go toward wall)  ROLLING (tumbling and EAPING)  (selectine-glycoprotein)  ADHESION (integrine-Ig)  TRANSMIGRATION (DIAPEDESIS)(PCAM)  Chemotaxis Definition: Is the directed movement of neutrophilis and macrophages in the area of inflammation towards the irritant depending on 1- exogenous bacteria product 2- endogenous mediators as complement, arachidonic acid metabolites and chemokines. Those lead to polimerization of actin and facilitation of movement LEUKOCYTE “ACTIVATION”  “triggered” by the offending stimuli for PMNs to: 1) Produce eicosanoids 2) Undergo DEGRANULATION 3) Secrete CYTOKINES  Phagocytosis Major benefit Definition: is the ingestion and destruction of bacteria, necrotic debris and foreign particles by the phagocytic inflammatory cells. Phagocytes Neutrophilis Macrophages 1- Recognition Opsonin(Ig, complement) 2- Engulfment 3- Killing and degradation (Oxidative and non-oxidative) Chemical MEDIATORS  Cellular  Plasma  HISTAMINE  COMPLEMENT  SEROTONIN  KININS  EICOSANOIDS  CLOTTING FACTORS  NITRIC OXIDE  Fibrinolytic  PLATELET ACTIVATING FACTOR (PAF)  Resolution Outcome of acute Regression & Healing inflammation Progression & spread Progression & Chronicity Summary of SEQUENCE OF EVENTS  VASODILATATION   INCREASED VASCULAR PERMEABILITY   LEAKAGE OF EXUDATE, stasis   Extravasation, MARGINATION, ROLLING, ADHESION, TRANSMIGRATION (DIAPEDESIS)   CHEMOTAXIS   PMN ACTIVATION   PHAGOCYTOSIS: Recognition,(Attachment), Engulfment, Killing (degradation or digestion)   TERMINATION 100% RESOLUTION, SCAR, or CHRONIC INFLAMMATION are the three possible outcomes  Types of acute inflammation acute inflammation Suppurative Non-Suppurative  Types of Acute Suppurative inflammation Suppurative inflammation Localised Diffuse Abscess Furuncle Carbuncle Cellulitis Characters and composition of pus  Non-coagulable creamy alkaline yellowish or yellow green fluid formed of:  1- fluid exudate without fibrin  2- pus cells, PNL, macropheges, RBCs  3- Liquified necrotic tissue  4- Bacteria and pigment  Abscess  Definition Localized suppurative acute inflammation  Cause Staph----Excess fibrin  Site: Skin, organs  Microscopically:  1-Central zone of necrotic tissue and dead neutrophils.b.  2-Peripheral zone of inflamed tissue.  3- granulation tissue---fibrosis  Clinical red, hot, swollen, Pus  Fate: Heal, complications  PUS = PURULENT ABSCESS = POCKET OF PUS PURULENT, FIBRINOPURULENT Boil-Furuncle  Small abscess related to hair follicle or sebaceous gland Carbuncle multiple communicating abscess Risk: Diabetics Site: back of neck Diffuse suppurative Inflammation  Causative organism:streptococcus haemolyticus producing  Enzyme 1-fibrinolysin, hyalouronidase and 2-spreading factor  Examples:  Cellulitis  Appendicitis  Peritonitis  Abscess Cellulitis Def Localized suppurative Diffuse suppurative examination examination Causative organism Staph Strept Mechanism Excess fibrin fibrinolysin, hyalouronidase andspreading factor Site Any tissue Loose tissue Pus Thick yellow Thin sangonous Spread Less More common Types of Acute Non-Suppurative inflammation necrotizing Haemohrragic serous Non- Allergic Suppurative Fbrinous Membranous serofibrinous Catarrhal Types of Acute Non-Suppurative inflammation Catarrhal inflammation: Rhinitis, excess mucous Serous inflammation: Pleuritis, Excess watery fluid exudate Pseudoembranous: Diphteria, Fibrin patches Chronic inflammation CAUSES of CHRONIC INFLAMMATION 1) PERSISTENCE of Infection 2) PROLONGED EXPOSURE to insult Types Non-specific: follow acute Specific: granuloma GRANULOMAS  Def: Chronic specific inflammation with nodular collection of epitheliod cells , lymphocytes and giant cells  Etiology Infective Bacteria: TB, Leprosy, Syphilis Parasitic: Bilh, Leishmania Fungi: Madura foot Non-infective Selecosis, FB Unknown Chrons, Sarcoidosis Components of Granuloma  4 COMPONENTS  HISTIOS, epitheliod cells (main component)  “GIANT” CELLS Langhan’s FB  LYMPHS  FIBROBLASTS  Classification (types)of GRANULOMAS 1. Granuloma with caseation: TB 2. Granuloma without caseation: Sarcoidosis, Chron’s, BILH, Selicosis 3. Suppurative granuloma: Cat scrach disease,Lymphgranuloma 4. Foreign body granuloma: thread, silicon implant  Langhans giant cell Foreign body giant cell