Chronic Inflammation (power Point).ppt

CHRONIC INFLAMMATION Prof Nicholas A TITILOYE  Response of vascularised tissues to injury Eliminates noxious agents paving way for repair Excessive/inadequate reactions fatal  INFLAMMATIO N ACUTE CHRONIC Rapid onset Slow onset...

CHRONIC INFLAMMATION Prof Nicholas A TITILOYE  Response of vascularised tissues to injury Eliminates noxious agents paving way for repair Excessive/inadequate reactions fatal  INFLAMMATIO N ACUTE CHRONIC Rapid onset Slow onset Prolonged Brief duration Modulated Stereotyped Inflammatory cells, Exudation & Injury & Repair PMN emigration Neutrophils Varied cell response  CHRONIC INFLAMMATION Persistent infection Prolonged exposure to potentially toxic agents (endogenous/ exogenous toxins) Immune mediated inflammatory disease CELLS IN CHRONIC INFLAMMATION Macrophage Lymphocyte Plasma cell Eosinophil Neutrophil  MACROPHAGES Derived from blood monocytes Differentiate as tissue macrophages which are larger than blood monocytes Extravasation of monocytes is govern by the same factors that are involved in neutrophils emigration Macrophages are activated by variety of stimuli which include cytokines, bacterial endotoxins and other chemical mediators.  Activation leads to increase cell size, increased level of lysosomal enzymes, more active metabolism, and a greater ability to phagocytose and kill ingested microbes Activated macrophages secrete a wide variety of biological active products that if unchecked result in the tissue injury and fibrosis characteristic of chronic inflammation  In short lived inflammation, macrophages eventually dies or make their ways into lymphatic and lymph nodes However in chronic inflammation Macrophages accumulation persist  Reason for persistence of macrophages in chronic inflammation Continual recruitment of monocytes from circulation Local proliferation of macrophages after their emigration from the blood stream Immobilization of macrophages from the site of inflammation  FACTORS DETERMINING THE HISTOLOGIC PATTERN Inciting agent Time of observation Host immune status  HISTOLOGIC PATTERNS Macrophage rich Eosinophil rich Lympho/plasmacytic Mixed cell Granulomatous  GRANULOMA- AETIOPATHOGENESIS FOREIGN BODY (Low turnover) IMMUNE (High turnover)  GRANULOMA- HISTOLOGICAL TYPES Epithelioid cell i. Non-caseating ii. Caseating iii. Suppurative Diffuse CASEATION NECROSIS Hilar lymph node in tuberculosi s CASEATION NECROSIS Tuberculou s broncho- pneumonia EPITHELIOID CELL GRANULOMAS- non- caseous EPITHELIOID CELL GRANULOMAS- caseating  SEQUELAE Fibrosis Dystrophic calcification Aa amyloidosis Cancer Discussion  Write a short note on Giant cell  Discuss the pathogenesis of giant cell seen in Tuberculosis  Describe the histology of TB Granuloma Sarcoidosis Granuloma Foreign body Granuloma  What is the relationship of Lymphocytes and Macrophages in Granuloma formation THANK YOU FOR LISTENING