Pathology of Inflammation PDF

Pathology of Inflammation  Inflammation Definition: Inflammation is “dynamic response of vascularised living tissue to injury.” It is physiologic, protective response. Serves to bring defense & healing mechanisms to the site of injury.  Aim of Inflammation 1- Isolate injury...

Pathology of Inflammation  Inflammation Definition: Inflammation is “dynamic response of vascularised living tissue to injury.” It is physiologic, protective response. Serves to bring defense & healing mechanisms to the site of injury.  Aim of Inflammation 1- Isolate injury 2- destroy invading microorganisms 3- inactivate toxins 4- prepare the damaged tissue to repair and healing Causes of inflammation 1- Infections. 2- Trauma. 3- Physical injury (heat, radiation). 4 -Chemical injury. 5- Immune mediated. 6- Adjacent to necrotic tissue.  Cardinal signs of inflammation Calor : Warm – Hyperaemia. Rubor : Redness – Hyperaemia. Dolor : Pain – Nerve, Chemical med. Tumor : Swelling – Exudation Functio laesa: Loss of function  Types of Inflammation:  Acute: ◦ Suppurative: ◦ – Localized: abscess, furuncle and carbuncle. - Diffuse: Cellulites ◦ Non Suppurative    Acute Chronic Strong irritant Mild Rapid response Gradual Short duration Prolonged Healing (fibrosis) Vascular dilatation End arteritis obliterans Excess fluid exudate Scanty Polymorphs, Lymphocytes, plasma, eosinophils, macrophages, giant cells macrophages  Definition: Is a rapid host response serves to deliver leukocytes and plasma proteins, such as antibodies to sites of infection or tissue injury.  Tissue response  Two main component of tissue response (inflammation) 1- Vascular response 2- Cellular response  B A C D 1- immediate vasoconstriction B 2- Vasodilatation 3- Increased vascular permeability - Contraction of endothelial cells with increased inter- endothelial space mediated by histamine and bradykinin - Endothelial cell injury: Endothelial cells undergo necrosis and detachment by either direct effect of injurious agent or effect of neutrophils C adherent to the D wall. - Transcytosis: Caused by interconnected uncoated vesicles and vacuoles called “vesiculo- vacuolar organelles,that increase in size in inflammation. 4- Formation of inflammatory exudate  Inflammatory Fluid Exudate Mechanism Vascular permeability Osmotic pressure Capillary hydrostatic pressure Amount Tissue Irritant Lymphatic obstruction Variable Transudate Exudate s Definition An ultrafiltrate of blood A filtrate of blood plasma mixed with plasma inflammatory cells and cellular debris Capillary Normal Increased permeabilit y Compositio  Fluid low in protein  Fluid high in protein content > 3 n content < 3 gm/dl gm/dl  Clear  Turbid  Liquid (like serum)  viscous (like pus)  Sp. Gravity 1.020  Scant cellular content  Contains numerous neutrophils Exudate Exudate and and Transudate Transudate Variables Transudate Exudate Definition Oedema fluid Inflammation fluid Capillary Normal Increased permeabili ty Compositio  Fluid low in protein  Fluid high in protein n content < 3 gm/dl content > 3 gm/dl  Clear  Turbid  Liquid (like serum)  viscous (like pus)  Sp. Gravity 1020  Scant cellular  Contains numerous content neutrophils Extravasation of cells is divided into three steps I – Intravascular: Margination Rolling and adhesion of leukocytes to the endothelium Transmigration across the endothelium II- Extravascular Chemotaxis Phagocytosis  Margination: due to stasis  Vasoconstriction Vasodilatation Stasis Exudation – Edema Emigration of cells Chemotaxis Phagocytosis  Rolling: occurs by P-& E- selectin on endothelial cells and oligosaccharides on leukocytes Stable adhesion depnd on Immunoglobulin family include ICAM-1 and VCAM-1 on endothelial cells and integrins on leukocytes Transmigration (diapedesis) depend on CD31 (PECAM-1) on both endothelial and leukocytes  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.  Phagocytosis Definition: is the ingestion and destruction of bacteria, necrotic debris and foreign particles by the phagocytic.inflammatory cells It is similar to the feeding process of amoeba Neutrophilis Macrophages 1- Recognition 2- Engulfment 3- Killing and degradation  1- Suppurative inflammation (1) Localized @ (A)Abscess: Definiti Abscess is a type of localized suppurative inflammation characterized by the formation of a cavity containing pus. Causes: It is commonly caused by staphylococcal infection. Site: It can occur in any organ, but is most common in the subcutaneous tissues. Characters and composition of pus: Pus is formed of: 1- Fluid exudate without fibrin (liquefied). 2- A large number of pus cells, neutrophils, 3- Necrotic fragments (sloughs) and liquefied necrotic tissue 4- Bacteria and bacterial pigments. (2) Diffuse  Caused by streptococcus haemolyticus bacteria which produce hyaluronidase (the spreading factor) and streptokinase (fibrinolysin) with dissolves fibrin.  The most common forms of diffuse suppurative inflammation are: a) Cellulitis: is common in diabetics b) Suppurative appendicitis. c) Septic peritonitis  Abscess Abscess and and Cellulitis Cellulitis Variables Abscess Cellulitis Definition Localized suppurative Diffuse suppurative inflammation inflammation Etiology Staph aureus Strepthemolyticus Produces coagulase Produces fibrinolysis and that localizes the hyalouronidase that lyses fibrin infection Site Any organ, commonly Loose connective tissue, orbit subcutaneous tissue areolar tissue, pelvis, and scrotum Pus is Thick (more liquefied Thin (less liquefied fibrin) fibrin) Many RBCs Few RBCs Spread of Less common More common inflammation  2-Non suppurative inflammation 1- Catarrhal (rhinitis, appendicitis) 2- Memmberanous(diphteria) 3- Sero-fibrinous (serous membranes) 4- Fibrinous(lobar pneumonia) 5- Serous (burn, herpes) 6- Haemorrhagic (hamolyt. Strept. Infect.) 7-Necrotizing (cancerum oris) 8-Allergic (anaphylactic shock, Br.asthma)  Chronic inflammation Character: Mild irritant with long duration. Follow acute inflammation or start as chronic. Mild vascular congestion and dilatation. Scanty fluid exudate. Healing by fibrosis. Chronic inflammatory cells; @lymphocytes @ plasma cells @Macrophages @ giant cell  Types Non-specific – Chronic abscess Specific (granuloma) – Tuberculosis or bilharziasis  Granuloma Type of chronic specific inflammation Collection of large number of : macrophages, lymphocytes, plasma, giant cells and fibroblasts Forming tiny microscopic granules Fuse to form tumor-like mass  Types Infective - Bacterial: T.B.,leprosy, syphilis. - Parasitic: Bilharziasis. - Fungal:Madura foot, histoplasmosis. Non Infective - Silicosis and asbestosis. Granuloma of unknowen cause: Sarcoidosis