ACUTE INFLAMMATION.pptx

ACUTE INFLAMMATION Prof. Nicholas Akinwale TITILOYE MBChB, FMCPath, FICS Dept of Pathology, Kwame Nkrumah University of Science and Technology. Kumasi INFLAMMATION  Inflammation is the response of vascularised connective tissue to inju...

ACUTE INFLAMMATION Prof. Nicholas Akinwale TITILOYE MBChB, FMCPath, FICS Dept of Pathology, Kwame Nkrumah University of Science and Technology. Kumasi INFLAMMATION  Inflammation is the response of vascularised connective tissue to injurious agents.  Even when there is injury or cell death as a result of the injury, inflammation is the body response.  Inflammation is characterised by extravasation of protein rich fluid and leukocyte in order to eliminate the offending agent.  KEYWORD 1. RESPONSE 2. VASCULARISED CONNECTIVE TISSUE / LIVING TISSUE 3. INJURIOUS AGENTS/INJURY/CELLULAR DEATH 4. FLUID AND LEUCOCYTE EXTRAVASATION Inflammation  Inflammation is an immune response, constitute a component of innate immune response  The aim is to protect tissue from damage  Regardless of the type of injurious agent, inflammation is the first response.  It occur without prior sensitization.  Inflammation is followed by adaptive /acquired Immune response, a specific response directed against foreign cells/antigens recognized by the body as “non self”. Aim of inflammation  Inflammation is complex reaction involving many cells and factors; a highly coordinated reaction.  It could be likened to an orchestral with the final aim targeted at dilution and destruction or walling off the injurious agent.  Inflammation consists of vascular responses, cellular response (migration and activation by leukocytes), and systemic reactions. Components of acute inflammation Steps in inflammation  Recognition of offending agent by host cells and molecules  Recruitment of inflammatory cells and exudates to the site  Activation of inflammatory cells and proteins  Termination of reaction  Repair of damage tissue EXUDATES IN INFLAMMATION  The fluid exudates in inflammation functions to:  Dilute irritants in tissues.  Form fibrin clot to provide scaffolding between severed tissues, to stop bleeding and to assist in phagocytosis.  Release natural anti-microbial substances: opsonins and immunoglobulins. ROLE OF THE CELLS  Release of chemicals that plays vital roles in inflammation  Phagocytosis of the injurious agents  Walling off of the injurious agents HISTORICALLY  Paul Ehrlich 1876 Mast cells  Elie Metchnikoff 1882 Phagocytosis in star fish larvae  Leber 1888 Bacteria induced chemotaxis  Metchnikoff & Ehrlich 1908 Nobel Prize in Physiology and Medicine  Ludwig Aschoff 1924 Reticuloendothelial system  Sir Thomas Lewis 1927 Role of chemical mediators  Dumonde and co-workers 1969 Lymphokines  Cohen and co-workers 1974 Cytokines  Aarden and co-workers 1979 Interleukins Nomenclature and Types of Inflammation  Diseases associated with inflammatory diseases are usually denoted by adding the suffix ‘itis’. For instance, the term meningitis refers to the inflammation of the meninges of the brain.  Inflammation can be divided into acute, or chronic Distinguishing factors in acute and chronic inflammation  the temporal aspects of the process  the intensity and severity of the initiating insult,  the type of cellular infiltrate characterizing the lesion or  the specific etiologic agent involved  (Usually) by a combination of all these factors. Acute/chronic inflammation  Chronic inflammation is a prolonged inflammation where healing has started  The onset of acute inflammation is rapid while that of chronic inflammation is slow  Response in acute inflammation is more stereotypic than chronic inflammation  While acute is characterized by inflammatory exudate, chronic inflammation is characterized by presence of cells and granulation tissue Chronic inflammation  Ongoing destruction and repair is seen in chronic inflammation  Chronic inflammation may be non specific  Or specific also called granulomatous reaction  Acute inflammation  Is a rapid response to an injurious agent that serves to deliver mediators of host defense – leukocytes and plasma proteins – to the site of injury. It has 3 major components;  Alteration in vascular caliber that leads to an increase in blood flow  Structural changes in the microvasculature that permits plasma proteins and leukocytes to leave the circulations.  Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agents Exudates and transudate  Exudates – is an inflammatory extra vascular fluid rich in plasma protein, cellular debris and has a specific gravity > 1.020.  Transudate – is a fluid low in protein and specific gravity